Biosubjetividades Biosubjectivities Biosubjectivités

Your brain on androids.

2011-07-18T09:04:00.000-07:00

Your brain on androids.
July 14th, 2011 in Neuroscience

Brain response to videos of a robot, android and human. The researchers say they see, in the android condition, evidence of a mismatch between the human-like appearance of the android and its robotic motion. Credit: Courtesy Ayse Saygin, UC San Diego

Ever get the heebie-jeebies at a wax museum? Feel uneasy with an anthropomorphic robot? What about playing a video game or watching an animated movie, where the human characters are pretty realistic but just not quite right and maybe a bit creepy? If yes, then you've probably been a visitor to what's called the "uncanny valley."

The phenomenon has been described anecdotally for years, but how and why this happens is still a subject of debate in robotics, computer graphics and neuroscience. Now an international team of researchers, led by Ayse Pinar Saygin of the University of California, San Diego, has taken a peek inside the brains of people viewing videos of an uncanny android (compared to videos of a human and a robot-looking robot).

Published in the Oxford University Press journal Social Cognitive and Affective Neuroscience, the functional MRI study suggests that what may be going on is due to a perceptual mismatch between appearance and motion.

The term "uncanny valley" refers to an artificial agent's drop in likeability when it becomes too humanlike. People respond positively to an agent that shares some characteristics with humans – think dolls, cartoon animals, R2D2. As the agent becomes more human-like, it becomes more likeable. But at some point that upward trajectory stops and instead the agent is perceived as strange and disconcerting. Many viewers, for example, find the characters in the animated film "Polar Express" to be off-putting. And most modern androids, including the Japanese Repliee Q2 used in the study here, are also thought to fall into the uncanny valley.

Saygin and her colleagues set out to discover if what they call the "action perception system" in the human brain is tuned more to human appearance or human motion, with the general goal, they write, "of identifying the functional properties of brain systems that allow us to understand others' body movements and actions."

They tested 20 subjects aged 20 to 36 who had no experience working with robots and hadn't spent time in Japan, where there's potentially more cultural exposure to and acceptance of androids, or even had friends or family from Japan.

The subjects were shown 12 videos of Repliee Q2 performing such ordinary actions as waving, nodding, taking a drink of water and picking up a piece of paper from a table. They were also shown videos of the same actions performed by the human on whom the android was modeled and by a stripped version of the android – skinned to its underlying metal joints and wiring, revealing its mechanics until it could no longer be mistaken for a human. That is, they set up three conditions: a human with biological appearance and movement; a robot with mechanical appearance and mechanical motion; and a human-seeming agent with the exact same mechanical movement as the robot.

At the start of the experiment, the subjects were shown each of the videos outside the fMRI scanner and were informed about which was a robot and which human.

The biggest difference in brain response the researchers noticed was during the android condition – in the parietal cortex, on both sides of the brain, specifically in the areas that connect the part of the brain's visual cortex that processes bodily movements with the section of the motor cortex thought to contain mirror neurons (neurons also known as "monkey-see, monkey-do neurons" or "empathy neurons").

According to their interpretation of the fMRI results, the researchers say they saw, in essence, evidence of mismatch. The brain "lit up" when the human-like appearance of the android and its robotic motion "didn't compute."

"The brain doesn't seem tuned to care about either biological appearance or biological motion per se," said Saygin, an assistant professor of cognitive science at UC San Diego and alumna of the same department. "What it seems to be doing is looking for its expectations to be met – for appearance and motion to be congruent."

In other words, if it looks human and moves likes a human, we are OK with that. If it looks like a robot and acts like a robot, we are OK with that, too; our brains have no difficulty processing the information. The trouble arises when – contrary to a lifetime of expectations – appearance and motion are at odds.

"As human-like artificial agents become more commonplace, perhaps our perceptual systems will be re-tuned to accommodate these new social partners," the researchers write. "Or perhaps, we will decide it is not a good idea to make them so closely in our image after all."

Saygin thinks it's "not so crazy to suggest we brain-test-drive robots or animated characters before spending millions of dollars on their development."

It's not too practical, though, to do these test-drives in expensive and hard-to-come-by fMRI scanners. So Saygin and her students are currently on the hunt for an analogous EEG signal. EEG technology is cheap enough that the electrode caps are being developed for home use.

Provided by University of California - San Diego

Risk factors predictive of psychiatric symptoms after traumatic brain injury

2011-07-18T07:59:00.000-07:00

Risk factors predictive of psychiatric symptoms after traumatic brain injury.

July 12th, 2011 in Psychology & Psychiatry.

A history of psychiatric illness such as depression or anxiety before a traumatic brain injury (TBI), together with other risk factors, are strongly predictive of post-TBI psychiatric disorders, according to an article published in Journal of Neurotrauma.

In addition to a pre-injury psychiatric disorder, two other factors are early indicators of an increased risk for psychiatric illness one year after a TBI: psychiatric symptoms during the acute post-injury period, and a concurrent limb injury. Kate Rachel Gould, DPsych, Jennie Louise Ponsford, PhD, Lisa Johnston, PhD, and Michael Schönberger, PhD, Epworth Hospital and Monash University, Melbourne, Australia, and University of Freiburg, Baden-Württemberg, Germany, also describe a link between risk of psychiatric symptoms and unemployment, pain, and poor quality of life during the 12-month post-TBI period.

In the presence of a limb injury, patients who suffered a TBI had a 6.4 greater risk of psychiatric disorders at 1 year, and a 4-fold greater risk of depression in particular, compared to patients without a limb injury. The authors report their findings in the article, "Predictive and Associated Factors of Psychiatric Disorders after Traumatic Brain Injury: A Prospective Study."

More information: The article is available free online at www.liebertpub.com/neu

Study demonstrates how memory can be preserved -- and forgetting prevented

2011-07-17T22:12:00.000-07:00

Study demonstrates how memory can be preserved -- and forgetting prevented
July 8th, 2011 in Neuroscience

As any student who's had to study for multiple exams can tell you, trying to learn two different sets of facts one after another is challenging. As you study for the physics exam, almost inevitably some of the information for the history exam is forgotten. It's been widely believed that this interference between memories develops because the brain simply doesn't have the capacity necessary to process both memories in quick succession. But is this truly the case?

A new study by researchers at Beth Israel Deaconess Medical Center (BIDMC) suggests that specific brain areas actively orchestrate competition between memories, and that by disrupting targeted brain areas through transcranial magnetic stimulation (TMS), you can preserve memory -- and prevent forgetting.

The findings are described in the June 26 Advance On-line issue of Nature Neuroscience.

"For the last 100 years, it has been appreciated that trying to learn facts and skills in quick succession can be a frustrating exercise," explains Edwin Robertson, MD, DPhil, an Associate Professor of Neurology at Harvard Medical School and BIDMC. "Because no sooner has a new memory been acquired than its retention is jeopardized by learning another fact or skill."

Robertson, together with BIDMC neurologist and coauthor Daniel Cohen, MD, studied a group of 120 college-age students who performed two concurrent memory tests. The first involved a finger-tapping motor skills task, the second a declarative memory task in which participants memorized a series of words. (Half of the group performed the tasks in this order, while a second group learned these same two tasks in reverse order.)

"The study subjects performed these back-to-back exercises in the morning," he explains. "They then returned 12 hours later and re-performed the tests. As predicted, their recall for either the word list or the motor-skill task had decreased when they were re-tested."

In the second part of the study, Robertson and Cohen administered TMS following the initial testing. TMS is a noninvasive technique that uses a magnetic simulator to generate a magnetic field that can create a flow of current in the brain.

"Because brain cells communicate through a process of chemical and electrical signals, applying a mild electrical current to the brain can influence the signals," Robertson explains. In this case, the researchers targeted two specific brain regions, the dorsolateral prefrontal cortex and the primary motor cortex. They discovered that by applying TMS to specific brain areas, they were able to reduce the interference and competition between the motor skill and word-list tasks and both memories remained intact.

"This elegant study provides fundamental new insights into the way our brain copes with the challenge of learning multiple skills and making multiple memories," says Alvaro Pascual-Leone, MD, PhD, Director of the Berenson-Allen Center for Noninvasive Brain Stimulation at BIDMC. "Specific brain structures seem to carefully balance how much we retain and how much we forget. Learning and remembering is a dynamic process and our brain devotes resources to keep the process flexible. By better understanding this process, we may be able to find novel approaches to help enhance learning and treat patients with memory problems and learning disabilities."

"Our observations suggest that distinct mechanisms support the communication between different types of memory processing," adds Robertson. "This provides a more dynamic and flexible account of memory organization than was previously believed. We've demonstrated that the interference between memories is actively mediated by brain areas and so may serve an important function that has previously been overlooked."

Provided by Beth Israel Deaconess Medical Center

Nueva Pagina del Instituto de Neuroartes en Facebook

2011-07-17T21:55:00.000-07:00

New gene for intellectual disability discovered

2011-07-17T21:54:00.001-07:00

New gene for intellectual disability discovered
July 15th, 2011 in Genetics

A gene linked to intellectual disability was found in a study involving the Centre for Addiction and Mental Health (CAMH) – a discovery that was greatly accelerated by international collaboration and new genetic sequencing technology, which is now being used at CAMH.

CAMH Senior Scientist Dr. John Vincent and colleagues identified defects on the gene, MAN1B1, among five families in which 12 children had intellectual disability. The results will be published in the July issue of the American Journal of Human Genetics.

Intellectual disability is a broad term describing individuals with limitations in mental abilities and in functioning in daily life. It affects one to three per cent of the population, and is often caused by genetic defects.

The individuals affected had similar physical features, and all had delays in walking and speaking. Some learned to care for themselves, while others needed help bathing and dressing. In addition, some had epilepsy or problems with overeating.

All were found to have two copies of a defective MAN1B1 gene, one inherited from each parent. These were different types of mutations on the same gene – yet the outcome, intellectual disability, was the same in different families – confirming that this gene was the cause of the disorder.

"This mutation was seen in five families, which is one of the most seen so far for genes causing this form of recessive intellectual disability," said Dr. Vincent, who last year made a breakthrough by identifying the PTCHD1 gene responsible for autism.

MAN1B1 codes an enzyme that has a quality control function in cells. This enzyme is believed to have a role in "proofreading" specific proteins after they are created in cells, and then recycling faulty ones, rather than allowing them to be released from the cell into the body. With the defective gene, this does not occur.

"This is a process that occurs throughout a person's lifetime, and is probably involved in most tissues in the body, so it is surprising that the children affected didn't have more symptoms," said Dr. Vincent, who is also head of the Molecular Neuropsychiatry and Development Laboratory at CAMH.

The discovery benefited from collaboration and the availability of new technology. Initially, the CAMH-Pakistani research team identified four families in Pakistan with multiple affected family members. As there had been intermarriage among cousins in these families, it enabled the researchers to begin mapping genes in particular regions of risk.

By teaming up with researchers from the Max Planck Institute in Berlin, Germany, conducting similar work on a family in Iran, they were able to focus on three genes of interest. These three genes were identified using next-generation sequencing, which sped the process in identifying the MAN1B1 gene. In addition, a University of Georgia scientist, Dr. Kelley Moremen, recreated one of the mutations in MAN1B1 in cells, which resulted in 1300-fold decrease in enzyme activity.

To date, MAN1B1 is the eighth known gene connected with recessive intellectual disability, but there are likely many more involved. "We would like to screen children with intellectual disability in a western population," said Dr. Vincent.

Provided by Centre for Addiction and Mental Health

"New gene for intellectual disability discovered." July 15th, 2011. http://medicalxpress.com/news/2011-07-gene-intellectual-disability.html

When the brain remembers but the patient doesn't.

2011-07-15T07:56:00.001-07:00

When the brain remembers but the patient doesn't
July 14th, 2011 in Neuroscience

Brain damage can cause significant changes in behaviour, such as loss of cognitive skills, but also reveals much about how the nervous system deals with consciousness. New findings reported in the July 2011 issue of Elsevier's Cortex demonstrate how the unconscious brain continues to process information even when the conscious brain is incapacitated.

Dr Stéphane Simon and collaborators in Professor Alan Pegna's laboratory at Geneva University Hospital, studied a patient brain damaged in an accident who had developed prosopagnosia, or face blindness. They measured her non-conscious responses to familiar faces, using different physiological measures of brain activity, including fMRI and EEG. The patient was shown photographs of unknown and famous people, some of whom were famous before the onset of her prosopagnosia (and others who had become famous more recently). Despite the fact that the patient could not recognize any of the famous faces, her brain activity responded to the faces that she would have recognized before the onset of her condition.

"The results of this study demonstrate that implicit processing might continue to occur despite the presence of an apparent impairment in conscious processing," says Professor Pegna, "The study has also shed light on what is required for our brain to understand what we see around us. Together with other research findings, this study suggests that the collaboration of several cerebral structures in a specific temporal order is necessary for visual awareness to arise."

More information: "When the brain remembers, but the patient doesn't: Converging fMRI and EEG evidence for covert recognition in a case of prosopagnosia" Cortex, Volume 47, Issue 7 (July 2010),

An account of the path to realizing tools for controlling brain circuits with light

2011-07-07T08:45:00.000-07:00

The Birth of Optogenetics

An account of the path to realizing tools for controlling brain circuits with light

By Edward S. Boyden | July 1, 2011Blue light hits a neuron engineered to express opsin molecules on its surface, opening a channel through which ions pass into the cell—activating the neuron.MIT McGovern Institute, Julie Pryor, Charles Jennings, Sputnik Animation, Ed Boyden

For a few years now, I’ve taught a course at MIT called “Principles of Neuroengineering.” The idea of the class is to get students thinking about how to create neurotechnology innovations—new inventions that can solve outstanding scientific questions or address unmet clinical needs. Designing neurotechnologies is difficult because of the complex properties of the brain: its inaccessibility, heterogeneity, fragility, anatomical richness, and high speed of operation. To illustrate the process, I decided to write a case study about the birth and development of an innovation with which I have been intimately involved: optogenetics—a toolset of genetically encoded molecules that, when targeted to specific neurons in the brain, allow the activity of those neurons to be driven or silenced by light.
A strategy: controlling the brain with light

As an undergraduate at MIT, I studied physics and electrical engineering and got a good deal of firsthand experience in designing methods to control complex systems. By the time I graduated, I had become quite interested in developing strategies for understanding and engineering the brain. After graduating in 1999, I traveled to Stanford to begin a PhD in neuroscience, setting up a home base in Richard Tsien’s lab. In my first year at Stanford I was fortunate enough to meet many nearby biologists willing to do collaborative experiments, ranging from attempting the assembly of complex neural circuits in vitro to behavioral experiments with rhesus macaques. For my thesis work, I joined the labs of Richard Tsien and of Jennifer Raymond in spring 2000, to study how neural circuits adapt in order to control movements of the body as the circumstances in the surrounding world change.

In parallel, I started thinking about new technologies for controlling the electrical activity of specific neuron types embedded within intact brain circuits. That spring, I discussed this problem—during brainstorming sessions that often ran late into the night—with Karl Deisseroth, then a Stanford MD-PhD student also doing research in Tsien’s lab. We started to think about delivering stretch-sensitive ion channels to specific neurons, and then tethering magnetic beads selectively to the channels, so that applying an appropriate magnetic field would result in the bead’s moving and opening the ion channel, thus activating the targeted neurons.

By late spring 2000, however, I had become fascinated by a simpler and potentially easier-to-implement approach: using naturally occurring microbial opsins, which would pump ions into or out of neurons in response to light. Opsins had been studied since the 1970s because of their fascinating biophysical properties, and for the evolutionary insights they offer into how life forms use light as an energy source or sensory cue.1 These membrane-spanning microbial molecules—proteins with seven helical domains—react to light by transporting ions across the lipid membranes of cells in which they are genetically expressed. (See the illustration above.) For this strategy to work, an opsin would have to be expressed in the neuron’s lipid membrane and, once in place, efficiently perform this ion-transport function. One reason for optimism was that bacteriorhodopsin had successfully been expressed in eukaryotic cell membranes—including those of yeast cells and frog oocytes—and had pumped ions in response to light in these heterologous expression systems. And in 1999, researchers had shown that, although many halorhodopsins might work best in the high salinity environments in which their host archaea naturally live (i.e., in very high chloride concentrations), a halorhodopsin from Natronomonas pharaonis (Halo/NpHR) functioned best at chloride levels comparable to those in the mammalian brain.

I was intrigued by this, and in May 2000 I e-mailed the opsin pioneer Janos Lanyi, asking for a clone of the N. pharaonis halorhodopsin, for the purpose of actively controlling neurons with light. Janos kindly asked his collaborator Richard Needleman to send it to me. But the reality of graduate school was setting in: unfortunately, I had already left Stanford for the summer to take a neuroscience class at the Marine Biology Laboratory in Woods Hole. I asked Richard to send the clone to Karl. When I returned to Stanford in the fall, I was so busy learning all the skills I would need for my thesis work on motor control that the opsin project took a backseat for a while.
The channelrhodopsin collaboration

In 2002 a pioneering paper from the lab of Gero Miesenböck showed that genetic expression of a three-gene Drosophila phototransduction cascade in neurons allowed the neurons to be excited by light, and suggested that the ability to activate specific neurons with light could serve as a tool for analyzing neural circuits.3 But the light-driven currents mediated by this system were slow, and this technical issue may have been a factor that limited adoption of the tool.

This paper was fresh in my mind when, in fall 2003, Karl e-mailed me to express interest in revisiting the magnetic-bead stimulation idea as a potential project that we could pursue together later—when he had his own lab, and I had finished my PhD and could join his lab as a postdoc. Karl was then a postdoctoral researcher in Robert Malenka’s lab (also at Stanford), and I was about halfway through my PhD. We explored the magnetic-bead idea between October 2003 and February 2004. Around that time I read a just-published paper by Georg Nagel, Ernst Bamberg, Peter Hegemann, and colleagues, announcing the discovery of channelrhodopsin-2 (ChR2), a light-gated cation channel and noting that the protein could be used as a tool to depolarize cultured mammalian cells in response to light.4

In February 2004, I proposed to Karl that we contact Georg to see if they had constructs they were willing to distribute. Karl got in touch with Georg in March, obtained the construct, and inserted the gene into a neural expression vector. Georg had made several further advances by then: he had created fusion proteins of ChR2 and yellow fluorescent protein, in order to monitor ChR2 expression, and had also found a ChR2 mutant with improved kinetics. Furthermore, Georg commented that in cell culture, ChR2 appeared to require little or no chemical supplementation in order to operate (in microbial opsins, the chemical chromophore all-trans-retinal must be attached to the protein to serve as the light absorber; it appeared to exist at sufficient levels in cell culture).

Finally, we were getting the ball rolling on targetable control of specific neural types. Karl optimized the gene expression conditions, and found that neurons could indeed tolerate ChR2 expression. Throughout July, working in off-hours, I debugged the optics of the Tsien-lab rig that I had often used in the past. Late at night, around 1 a.m. on August 4, 2004, I went into the lab, put a dish of cultured neurons expressing ChR2 into the microscope, patch-clamped a glowing neuron, and triggered the program that I had written to pulse blue light at the neurons. To my amazement, the very first neuron I patched fired precise action potentials in response to blue light. That night I collected data that demonstrated all the core principles we would publish a year later in Nature Neuroscience, announcing that ChR2 could be used to depolarize neurons.5 During that long, exciting first night of experimentation in 2004, I determined that ChR2 was safely expressed and physiologically functional in neurons. The neurons tolerated expression levels of the protein that were high enough to mediate strong neural depolarizations. Even with brief pulses of blue light, lasting just a few milliseconds, the magnitude of expressed-ChR2 photocurrents was large enough to mediate single action potentials in neurons, thus enabling temporally precise driving of spike trains. Serendipity had struck—the molecule was good enough in its wild-type form to be used in neurons right away. I e-mailed Karl, “Tired, but excited.” He shot back, “This is great!!!!!”

Transitions and optical neural silencers

In January 2005, Karl finished his postdoc and became an assistant professor of bioengineering and psychiatry at Stanford. Feng Zhang, then a first-year graduate student in chemistry (and now an assistant professor at MIT and at the Broad Institute), joined Karl’s new lab, where he cloned ChR2 into a lentiviral vector, and produced lentivirus that greatly increased the reliability of ChR2 expression in neurons. I was still working on my PhD, and continued to perform ChR2 experiments in the Tsien lab. Indeed, about half the ChR2 experiments in our first optogenetics paper were done in Richard Tsien’s lab, and I owe him a debt of gratitude for providing an environment in which new ideas could be pursued. I regret that, in our first optogenetics paper, we did not acknowledge that many of the key experiments had been done there. When I started working in Karl’s lab in late March 2005, we carried out experiments to flesh out all the figures for our paper, which appeared in Nature Neuroscience in August 2005, a year after that exhilarating first discovery that the technique worked.

Around that same time, Guoping Feng, then leading a lab at Duke University (and now a professor at MIT), began to make the first transgenic mice expressing ChR2 in neurons.6 Several other groups, including the Yawo, Herlitze, Landmesser, Nagel, Gottschalk, and Pan labs, rapidly published papers demonstrating the use of ChR2 in neurons in the months following.7,8,9,10 Clearly, the idea had been in the air, with many groups chasing the use of channelrhodopsin in neurons. These papers showed, among many other groundbreaking results, that no chemicals were needed to supplement ChR2 function in the living mammalian brain.

Almost immediately after I finished my PhD in October 2005, two months after our ChR2 paper came out, I began the faculty job search process. At the same time, I started a position as a postdoctoral researcher with Karl and with Mark Schnitzer at Stanford. The job-search process ended up consuming much of my time, and being on the road, I began doing bioengineering invention consulting in order to learn about other new technology areas that could be brought to bear on neuroscience. I accepted a faculty job offer from the MIT Media Lab in September 2006, and began the process of setting up a neuroengineering research group there.

Around that time, I began a collaboration with Xue Han, my then girlfriend (and a postdoctoral researcher in the lab of Richard Tsien), to revisit the original idea of using the N. pharaonis halorhodopsin to mediate optical neural silencing. Back in 2000, Karl and I had planned to pursue this jointly; there was now the potential for competition, since we were working separately. Xue and I ordered the gene to be synthesized in codon-optimized form by a DNA synthesis company, and, using the same Tsien-lab rig that had supported the channelrhodopsin paper, Xue acquired data showing that this halorhodopsin could indeed silence neural activity. Our paper11 appeared in the March 2007 issue of PLoS ONE; Karl’s group, working in parallel, published a paper in Nature a few weeks later, independently showing that this halorhodopsin could support light-driven silencing of neurons, and also including an impressive demonstration that it could be used to manipulate behavior in Caenorhabditis elegans.12 Later, both our groups teamed up to file a joint patent on the use of this halorhodopsin to silence neural activity. As a testament to the unanticipated side effects of following innovation where it leads you, Xue and I got married in 2009 (and she is now an assistant professor at Boston University).

I continued to survey a wide variety of microorganisms for better silencing opsins: the inexpensiveness of gene synthesis meant that it was possible to rapidly obtain genes codon-optimized for mammalian expression, and to screen them for new and interesting light-drivable neural functions. Brian Chow (now an assistant professor at the University of Pennsylvania) joined my lab at MIT as a postdoctoral researcher, and began collaborating with Xue. In 2008 they identified a new class of neural silencer, the archaerhodopsins, which were not only capable of high-amplitude neural silencing—the first such opsin that could support 100 percent shutdown of neurons in the awake, behaving animal—but also were capable of rapid recovery after having been illuminated for extended durations, unlike halorhodopsins, which took minutes to recover after long-duration illumination.13 Interestingly, the archaerhodopsins are light-driven outward pumps, similar to bacteriorhodopsin—they hyperpolarize neurons by pumping protons out of the cells. However, the resultant pH changes are as small as those produced by channelrhodopsins (which have proton conductances a million times greater than their sodium conductances), and well within the safe range of neuronal operation. Intriguingly, we discovered that the H. salinarum bacteriorhodopsin, the very first opsin characterized in the early 1970s, was able to mediate decent optical neural silencing, suggesting that perhaps opsins could have been applied to neuroscience decades ago.
Beyond luck: systematic discovery and engineering of optogenetic tools

An essential aspect of furthering this work is the free and open distribution of these optogenetic tools, even prior to publication. To facilitate teaching people how to use these tools, our lab regularly posts white papers on our website* with details on reagents and optical hardware (a complete optogenetics setup costs as little as a few thousand dollars for all required hardware and consumables), and we have also partnered with nonprofit organizations such as Addgene and the University of North Carolina Gene Therapy Center Vector Core to distribute DNA and viruses, respectively. We regularly host visitors to observe experiments being done in our lab, seeking to encourage the community building that has been central to the development of optogenetics from the beginning.

As a case study, the birth of optogenetics offers a number of interesting insights into the blend of factors that can lead to the creation of a neurotechnological innovation. The original optogenetic tools were identified partly through serendipity, guided by a multidisciplinary convergence and a neuroscience-driven knowledge of what might make a good tool. Clearly, the original serendipity that fostered the formation of this concept, and that accompanied the initial quick try to see if it would work in nerve cells, has now given way to the systematized luck of bioengineering, with its machines and algorithms designed to optimize the chances of finding something new. Many labs, driven by genomic mining and mutagenesis, are reporting the discovery of new opsins with improved light and color sensitivities and new ionic properties. It is to be hoped, of course, that as this systematized luck accelerates, we will stumble upon more innovations that can aid in dissecting the enormous complexity of the brain—beginning the cycle of invention again.
Putting the toolbox to work

These optogenetic tools are now in use by many hundreds of neuroscience and biology labs around the world. Opsins have been used to study how neurons contribute to information processing and behavior in organisms including C. elegans, Drosophila, zebrafish, mouse, rat, and nonhuman primate. Light sources such as conventional mercury and xenon lamps, light-emitting diodes, scanning lasers, femtosecond lasers, and other common microscopy equipment suffice for in vitro use.

In vivo mammalian use of these optogenetic reagents has been greatly facilitated by the availability of inexpensive lasers with optical-fiber outputs; the free end of the optical fiber is simply inserted into the brain of the live animal when needed,14 or coupled at the time of experimentation to an implanted optical fiber.

For mammalian systems, viruses bearing genes encoding for opsins have proven popular in experimental use, due to their ease of creation and use. These viruses achieve their specificity either by infecting only specific neurons, or by containing regulatory promoters that constrain opsin expression to certain kinds of neurons.

An increasing number of transgenic mouse lines are also now being created, in which an opsin is expressed in a given neuron type through transgenic methodologies. One popular hybrid strategy is to inject a virus that contains a Cre-activated genetic cassette encoding for the opsin into one of the burgeoning number of mice that express Cre recombinase in specific neuron types, so that the opsin will only be produced in Cre recombinase-expressing neurons. 15

In 2009, in collaboration with the labs of Robert Desimone and Ann Graybiel at MIT, we published the first use of channelrhodopsin-2 in the nonhuman primate brain, showing that it could safely and effectively mediate neuron type–specific activation in the rhesus macaque without provoking neuron death or functional immune reactions. 16 This paper opened up a possibility of translating the technique of optical neural stimulation into the clinic as a treatment modality, although clearly much more work is required to understand this potential application of optogenetics.

Edward Boyden leads the Synthetic Neurobiology Group at MIT, where he is the Benesse Career Development Professor and associate professor of biological engineering and brain and cognitive science at the MIT Media Lab and the MIT McGovern Institute.
References

D. Oesterhelt, W. Stoeckenius, “Rhodopsin-like protein from the purple membrane of Halobacterium halobium,” Nat New Biol, 233:149-52, 1971.
D. Okuno et al., “Chloride concentration dependency of the electrogenic activity of halorhodopsin,” Biochemistry, 38:5422-29, 1999.
B.V. Zemelman et al., “Selective photostimulation of genetically chARGed neurons,” Neuron, 33:15-22, 2002.
G. Nagel et al., “Channelrhodopsin-2, a directly light-gated cation-selective membrane channel,” PNAS, 100:13940-45, 2003.
E.S. Boyden et al., “Millisecond-timescale, genetically targeted optical control of neural activity,” Nat Neurosci, 8:1263-68, 2005.
B.R. Arenkiel et al., “In vivo light-induced activation of neural circuitry in transgenic mice expressing channelrhodopsin-2,” Neuron, 54:205-18, 2007.
T. Ishizuka et al., “Kinetic evaluation of photosensitivity in genetically engineered neurons expressing green algae light-gated channels,” Neurosci Res, 54:85-94, 2006.
X. Li et al., “Fast noninvasive activation and inhibition of neural and network activity by vertebrate rhodopsin and green algae channelrhodopsin,” PNAS, 102:17816-21, 2005.
G. Nagel et al., “Light activation of channelrhodopsin-2 in excitable cells of Caenorhabditis elegans triggers rapid behavioral responses,” Curr Biol, 15:2279-84, 2005.
A. Bi et al., “Ectopic expression of a microbial-type rhodopsin restores visual responses in mice with photoreceptor degeneration,” Neuron, 50:23-33, 2006.
X. Han, E.S. Boyden, “Multiple-color optical activation, silencing, and desynchronization of neural activity, with single-spike temporal resolution,” PLoS ONE, 2:e299, 2007.
F. Zhang et al., “Multimodal fast optical interrogation of neural circuitry,” Nature, 446:633-39, 2007.
B.Y. Chow et al., “High-performance genetically targetable optical neural silencing by light-driven proton pumps,” Nature, 463:98-102, 2010.
A.M. Aravanis et al., “An optical neural interface: in vivo control of rodent motor cortex with integrated fiberoptic and optogenetic technology,” J Neural Eng, 4:S143-56, 2007.
D.Atasoy et al., “A FLEX switch targets Channelrhodopsin-2 to multiple cell types for imaging and long-range circuit mapping,” J Neurosci, 28:7025-30, 2008.
X. Han et al., “Millisecond-Timescale Optical Control of Neural Dynamics in the Nonhuman Primate Brain,” Neuron, 62:191-98, 2009.

Chimps Are Good Listeners, Too.

2011-07-03T07:07:00.000-07:00

Chimps Are Good Listeners, Too.
by Michael Balter on 1 July 2011.

I can talk, too! Panzee can communicate with humans using a board filled with symbols.

Most researchers regard language as unique to humans, something that makes our species special. But they fiercely debate how the ability to speak and listen evolved. Did speech require our species to evolve novel capabilities, or did we simply combine and enhance various abilities that other animals have, too? A new study with a language-trained chimp suggests that when it comes to understanding speech, the basic equipment might already have been present in our apelike ancestors.

The notion that language evolved only in the human lineage and has no parallels in other animals has long been attributed to the linguist Noam Chomsky, who argued beginning in the 1960s that humans had a special "language organ" unique to us. But more recent studies have shown that other species are surprisingly good at communication, and many researchers have abandoned this idea—even Chomsky himself no longer holds to it strictly.

However, some scientists continue to argue that humans have evolved unique ways to perceive and understand speech that allows us to use words as symbols for complex meanings. These contentions are based in part on a notable human talent: We can recognize words and understand entire sentences, even if the sounds of the words have been dramatically altered until they are a pale shadow of their linguistically meaningful selves.

So a team of researchers turned to Panzee, a 25-year-old chimpanzee, to test the assumption that only humans have this talent. Humans raised Panzee from the age of 8 days, and her caregivers exposed her to a rich diet of English language conversation about food, people, objects, and events. Panzee can't talk, so she communicates with those around her using a lexigram board of symbols corresponding to English words (see photo). She can point to 128 different lexigrams when she hears the corresponding spoken word.

A team led by Lisa Heimbauer, a cognitive psychologist at Georgia State University in Atlanta, set out to see how well Panzee could duplicate the human talent of understanding English word sounds when they are so badly distorted that they are difficult to recognize. The team used two electronic methods to distort the words: noise-vocoded (NV) synthesis, which makes words sound very raspy and breathy; the other, known as sine-wave (SW) synthesis, which reduces words to just three tones, is something like converting a rich color photograph into a stripped-down black and white version. (The words included chimp-friendly terms such as banana, potato, tickle, and balloon.)

Panzee performed well above chance when she heard distorted versions of 48 words that she knew and had to choose among four lexigrams, the team reports this week in Current Biology. Thus, while a chance result would have been one out of four correct choices, or 25%, Panzee scored 55% with NV words and about 40% with SW words, which are particularly difficult to understand even for humans. This was almost as good as the performance of 32 human subjects using the same 48 words, who chose the correct NV word 70% of the time but, like Panzee, the correct SW word only 40% of the time.

Heimbauer and her colleagues say that Panzee's strong performance argues against the idea that humans evolved highly attuned speech-recognition abilities only after they split from the chimp line some 5 million to 7 million years ago. The finding that Panzee passed a challenging test for speech recognition implies, the team writes, that "even quite sophisticated human speech perception phenomena may be within reach for some nonhumans." Still, the team says that its experiments don't rule out that humans have evolved additional speech-perception abilities that our ancestors and chimps lacked.

The authors have come up with a "nice result," says biologist Johan Bolhuis of Utrecht University in the Netherlands, but it shouldn't come as "a big surprise." For example, zebra finches have been shown to be able to distinguish very small sound differences in words spoken by humans, including ones that differ by only one vowel. That's a talent Bolhuis considers "even more remarkable" than Panzee's because it so closely parallels the way humans perceive speech.

J.D. Trout, a psychologist and philosopher at Loyola University Chicago in Illinois, thinks that the authors are far from proving their case. "These experiments don't bear on the question of whether speech is a special adaptation of humans," Trout insists, noting that the human subjects had to pull matching words out of their vocabularies of about 30,000 words, whereas Panzee had a much smaller vocabulary to search through. But Heimbauer points out that unlike the human subjects, Panzee had never been exposed to distorted speech before the experiment, making her performance all the more impressive.

Researchers can predict future actions from human brain activity

2011-06-30T08:31:00.000-07:00

Researchers can predict future actions from human brain activity

Bringing the real world into the brain scanner, researchers at The University of Western Ontario from The Centre for Brain and Mind can now determine the action a person was planning, mere moments before that action is actually executed.

"Neuroimaging allows us to look at how action planning unfolds within human brain areas without having to insert electrodes directly into the human brain. This is obviously far less intrusive," explains Western Psychology professor Jody Culham, who was the paper's senior author.ls from many brain regions, they could predict, better than chance, which of the actions the volunteer was merely intending to do, seconds later.The findings were published this week in the prestigious Journal of Neuroscience, in the paper, "Decoding Action Intentions from Preparatory Brain Activity in Human Parieto-Frontal Networks."

"This is a considerable step forward in our understanding of how the human brain plans actions," says Jason Gallivan, a Western Neuroscience PhD student, who was the first author on the paper.

[This video is not supported by your browser at this time.]

University of Western Ontario researchers Jody Culham and Jason Gallivan describe how they can use a fMRI to determine the action a person was planning, mere moments before that action is actually executed. Credit: The University of Western Ontario
Over the course of the one-year study, human subjects had their brain activity scanned using functional magnetic resonance imaging (fMRI) while they performed one of three hand movements: grasping the top of an object, grasping the bottom of the object, or simply reaching out and touching the object. The team found that by using the signals from many brain regions, they could predict, better than chance, which of the actions the volunteer was merely intending to do, seconds later.

Gallivan says the new findings could also have important clinical implications: "Being able to predict a human's desired movements using brain signals takes us one step closer to using those signals to control prosthetic limbs in movement-impaired patient populations, like those who suffer from spinal cord injuries or locked-in syndrome."

Provided by University of Western Ontario

"Researchers can predict future actions from human brain activity." June 29th, 2011. http://medicalxpress.com/news/2011-06-future-actions-human-brain.html

Exhumation of Shakespeare to determine cause of death and drug test

2011-06-28T07:40:00.000-07:00

Director of the Institute for Human Evolution, anthropologist Francis Thackeray has formally petitioned the Church of England to allow him to exhume the body of William Shakespeare in order to determine the cause of his death.

Thackeray is best known for his controversial suggestion nearly a decade ago which pointed to the possibility that Shakespeare had been a regular cannabis smoker. Utilizing forensic techniques, Thackeray examined 24 pipes which had been discovered in Shakespeare’s garden and determined that they had been used to smoke the drug.

Citing that even after 400 years, Shakespeare is still one of the most famous people in history, Thackeray hopes to be able to end the question of how he died and establish a health history. With new state-of-the-art computer equipment he hopes to create a three dimensional reconstruction of Shakespeare. The hope is to be able to determine the kind of life he led, any diseases of medical conditions he may have suffered from and what ultimately caused his death.

The new technology, nondestructive analysis, will not require the remains to be moved but will instead scan the bones. They are also hoping to collect DNA from Shakespeare and his wife and sister, all who are buried at Holy Trinity Church.

Thackeray also hopes to find evidence to back his controversial claims years ago regarding Shakespeare’s marijuana smoking. Examining the teeth could provide the evidence they need. If they are able to discover grooves between the incisor and canine teeth, it could show them he was chewing on a pipe.

This plan however goes against the final wishes of Shakespeare himself who had the following words engraved on his tomb: “Good frend for Jesus sake forebeare, To dig the dust encloased heare, Bleste be the man that spares thes stones, And curst be he that moves my bones.”

The Church of England denies that any requests have been made to exhume Shakespeare’s body but Thackeray and his team hopes to gain approval in time to be able to make the determination before the 400th anniversary of his death in 2016.

A little practice can change the brain in a lasting way: study

2011-06-28T07:32:00.000-07:00

A little practice can change the brain in a lasting way: study
June 27th, 2011 in Psychology & Psychiatry

A little practice goes a long way, according to researchers at McMaster University, who have found the effects of practice on the brain have remarkable staying power.

The study, published this month in the journal Psychological Science, found that when participants were shown visual patterns—faces, which are highly familiar objects, and abstract patterns, which are much less frequently encountered—they were able to retain very specific information about those patterns one to two years later.

"We found that this type of learning, called perceptual learning, was very precise and long-lasting," says Zahra Hussain, lead author of the study who is a former McMaster graduate student in the Department of Psychology, Neuroscience & Behaviour and now a Research Fellow at the University of Nottingham. "These long-lasting effects arose out of relatively brief experience with the patterns – about two hours, followed by nothing for several months, or years."

Over the course of two consecutive days, participants were asked to identify a specific face or pattern from a larger group of images. The task was challenging because images were degraded—faces were cropped, for example—and shown very briefly. Participants had difficulty identifying the correct images in the early stages, but accuracy rates steadily climbed with practice.

About one year later, a group of participants were called back and their performance on the task was re-measured, both with the same set of items they'd been exposed to earlier, and with a new set from the same class of images. Researchers found that when they showed participants the original images, accuracy rates were high. When they showed participants new images, accuracy rates plummeted, even though the new images closely resembled the learned ones, and they hadn't seen the original images for at least a year.

"During those months in between visits to our lab, our participants would have seen thousands of faces, and yet somehow maintained information about precisely which faces they had seen over a year ago," says Allison Sekuler, co-author of the study and professor and Canada Research Chair in Cognitive Neuroscience in the Department of Psychology, Neuroscience & Behaviour. "The brain really seems to hold onto specific information, which provides great promise for the development of brain training, but also raises questions about what happens as a function of development. How much information do we store as we grow, older and how does the type of information we store chage across our lifetimes? And what is the impact of storing all that potentially irrelevant information on our ability to learn and remember more relevant information?"

She and her colleagues point to children today who are growing up in a world in which they are bombarded with sensory information, and wonders what will happen.

"We don't yet know the long-term implications of retaining all this information, which is why it is so important to understand the physiological underpinnings," says Patrick Bennett, co-author and professor and Canada Research Chair in Vision Science in the Department of Psychology, Neuroscience & Behaviour. "This result warrants further study on how we can optimize our ability to train the brain to preserve what would be considered the most valuable information."

More information: A pdf of the study can be found at: http://dailynews.m … SciFinal.pdf

Provided by McMaster University

Restoring memory, repairing damaged brains

2011-06-18T05:55:00.000-07:00

Restoring memory, repairing damaged brains

June 17th, 2011 in Neuroscience

In the experiment, the researchers had rats learn a task, pressing one lever rather than another to receive a reward. Using embedded electrical probes, the experimental research team recorded changes in the rat's brain activity between the two major internal divisions of the hippocampus, known as subregions CA3 and CA1. The experimenters then blocked the normal neural interactions between the two areas using pharmacological agents. The previously trained rats then no long displayed the long-term learned behavior. But long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function. Credit: USC Viterbi School of Engineering
Scientists have developed a way to turn memories on and off -- literally with the flip of a switch.

Using an electronic system that duplicates the neural signals associated with memory, they managed to replicate the brain function in rats associated with long-term learned behavior, even when the rats had been drugged to forget.

"Flip the switch on, and the rats remember. Flip it off, and the rats forget," said Theodore Berger of the USC Viterbi School of Engineering's Department of Biomedical Engineering.

Berger is the lead author of an article that will be published in the Journal of Neural Engineering. His team worked with scientists from Wake Forest University in the study, building on recent advances in our understanding of the brain area known as the hippocampus and its role in learning.

In the experiment, the researchers had rats learn a task, pressing one lever rather than another to receive a reward. Using embedded electrical probes, the experimental research team, led by Sam A. Deadwyler of the Wake Forest Department of Physiology and Pharmacology, recorded changes in the rat's brain activity between the two major internal divisions of the hippocampus, known as subregions CA3 and CA1. During the learning process, the hippocampus converts short-term memory into long-term memory, the researchers prior work has shown.

"No hippocampus," says Berger, "no long-term memory, but still short-term memory." CA3 and CA1 interact to create long-term memory, prior research has shown.

In a dramatic demonstration, the experimenters blocked the normal neural interactions between the two areas using pharmacological agents. The previously trained rats then no longer displayed the long-term learned behavior.

"The rats still showed that they knew 'when you press left first, then press right next time, and vice-versa,'" Berger said. "And they still knew in general to press levers for water, but they could only remember whether they had pressed left or right for 5-10 seconds."

Using a model created by the prosthetics research team led by Berger, the teams then went further and developed an artificial hippocampal system that could duplicate the pattern of interaction between CA3-CA1 interactions.

Long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function.

In addition, the researchers went on to show that if a prosthetic device and its associated electrodes were implanted in animals with a normal, functioning hippocampus, the device could actually strengthen the memory being generated internally in the brain and enhance the memory capability of normal rats.

"These integrated experimental modeling studies show for the first time that with sufficient information about the neural coding of memories, a neural prosthesis capable of real-time identification and manipulation of the encoding process can restore and even enhance cognitive mnemonic processes," says the paper.

Next steps, according to Berger and Deadwyler, will be attempts to duplicate the rat results in primates (monkeys), with the aim of eventually creating prostheses that might help the human victims of Alzheimer's disease, stroke or injury recover function.

The paper is entitled "A Cortical Neural Prosthesis for Restoring and Enhancing Memory." Besides Deadwyler and Berger, the other authors are, from USC, BME Professor Vasilis Z. Marmarelis and Research Assistant Professor Dong Song, and from Wake Forest, Associate Professor Robert E. Hampson and Post-Doctoral Fellow Anushka Goonawardena.

Berger, who holds the David Packard Chair in Engineering, is the Director of the USC Center for Neural Engineering, Associate Director of the National Science Foundation Biomimetic MicroElectronic Systems Engineering Research Center, and a Fellow of the IEEE, the AAAS, and the AIMBE

A fossil of modern humans, dating back 160,000 years.

2011-06-16T06:51:00.000-07:00

A fossil of modern humans, dating back 160,000 years.

At Britain's Royal Society, Dr. Marta Lahr from Cambridge University's Leverhulme Centre for Human Evolutionary Studies presented her findings that the height and brain size of modern-day humans is shrinking.

Looking at human fossil evidence for the past 200,000 years, Lahr looked at the size and structure of the bones and skulls found across Europe, Africa and Asia. What they discovered was that the largest Homo sapiens lived 20,000 to 30,000 years ago with an average weight between 176 and 188 pounds and a brain size of 1,500 cubic centimeters.

They discovered that some 10,000 years ago however, size started getting smaller both in stature and in brain size. Within the last 10 years, the average human size has changed to a weight between 154 and 176 pounds and a brain size of 1,350 cubic centimeters.

While large size remained static for close to 200,000 years, researchers believe the reduction in stature can be connected to a change from the hunter-gatherer way of life to that of agriculture which began some 9,000 years ago.

The fossilized skull of an adult male hominid unearthed in 1997 from a site near the village of Herto, Middle Awash, Ethiopia. The skull, reconstructed by UC Berkeley paleoanthropologist Tim White, is slightly larger than the most extreme adult male humans today, but in other ways is more similar to modern humans than to earlier hominids, such as the neanderthals. White and his team concluded that the 160,000 year old hominid is the oldest known modern human, which they named Homo sapiens idaltu. Image © J. Matternes
While the change to agriculture would have provided a plentiful crop of food, the limiting factor of farming may have created vitamin and mineral deficiencies and resulted in a stunted growth. Early Chinese farmers ate cereals such as rice which lacks the B vitamin niacin which is essential for growth.

Agriculture however does not explain the reduction in brain size. Lahr believes that this may be a result of the energy required to maintain larger brains. The human brain accounts for one quarter of the energy the body uses. This reduction in brain size however does not mean that modern humans are less intelligent. Human brains have evolved to work more efficiently and utilize less energy.

Brain structure adapts to environmental change

2011-06-14T05:19:00.000-07:00

Brain structure adapts to environmental change
June 13th, 2011 in Neuroscience

Scientists have known for years that neurogenesis takes place throughout adulthood in the hippocampus of the mammalian brain. Now Columbia researchers have found that under stressful conditions, neural stem cells in the adult hippocampus can produce not only neurons, but also new stem cells. The brain stockpiles the neural stem cells, which later may produce neurons when conditions become favorable. This response to environmental conditions represents a novel form of brain plasticity. The findings were published online in Neuron on June 9, 2011.

The hippocampus is involved in memory, learning, and emotion. A research team led by Alex Dranovsky, MD, PhD, assistant professor of clinical psychiatry at Columbia University Medical Center and research scientist in the Division of Integrative Neuroscience at the New York State Psychiatric Institute/Columbia Psychiatry, compared the generation of neural stem cells and neurons in mice housed in isolation and in mice housed in enriched environments. They then used lineage studies, a technique that traces stem cells from their formation to their eventual differentiation into specific cell types, to see what proportion of neural stem cells produced neurons.

Deprived and enriched environments had opposite effects. The brains of the socially isolated mice accumulated neural stem cells but not neurons. The brains of mice housed in enriched environments produced far more neurons, but not more stem cells. The average mouse dentate gyrus, the area of the hippocampus where neurogenesis takes place, has about 500,000 neurons; the enriched environment caused an increase of about 70,000 neurons.

"We already knew that enriching environments are neurogenic, but ours is the first report that neural stem cells, currently thought of as 'quiescent,' can accumulate in the live animal," said Dr. Dranovsky. "Since this was revealed simply by changing the animal's living conditions, we think that it is an adaptation to stressful environments. When conditions turn more favorable, the stockpiled stem cells have the opportunity to produce more neurons—a form of 'neurons on demand.'"

The researchers also looked at neuronal survival. They found that social isolation did not cause it to decrease. Scientists already knew that environmental enrichment increased neuronal survival―further increasing the neuron population.

To a lesser extent, location within the hippocampus affected whether stem cells became neurons. While the ratio of stem cells to neurons remained constant in the lower blade of the dentrate gyrus, it varied in the upper blade.

Age also affected the results. After three months, the brains of the isolated mice stopped accumulating neural stem cells. But the mice in enriched environments continued to produce more neurons.

Dranovsky and his team now want to see whether this hippocampal response is specific to social isolation or is a more general response to stress. Another question is whether all neural stem cells have the same potential to produce neurons.

"The long-term goal." Said Dr. Dranovsky, "is to figure out how to instruct neural stem cells to produce neurons or more stem cells. This could lead to the eventual use of stem cells in neuronal replacement therapy for neurodegenerative diseases and other central nervous system conditions."

Provided by Columbia University

Can Brain Scans Predict Music Sales?

2011-06-13T05:52:00.001-07:00

Can Brain Scans Predict Music Sales?
by Greg Miller on 10 June 2011, 11:35 AM

Rock my accumbens. A study inspired by a performance of OneRepublic's hit Apologize finds that activity in the nucleus accumbens correlates with music sales.
Credit: Kevin Winter/Tonight Show/Getty Images
Scientific inspiration sometimes comes from unlikely sources. Two years ago, Gregory Berns, a neuroeconomist at Emory University in Atlanta, was on the couch with his kids watching American Idol. One of the contestants sang the melancholy hit song Apologize by the alternative rock band OneRepublic, and something clicked in Berns's mind.

He'd used the song a few years earlier in a study on the neural mechanisms of peer pressure, in this case, how teenagers' perceptions of a song's popularity influence how they rate the song themselves. At the time, OneRepublic had yet to sign its first record deal. A student in Bern's lab had pulled a clip of Apologize from the band's MySpace page to use in the study. When Berns heard the song on American Idol, he wondered whether anything in the brain scan data his team had collected could have predicted it would become a hit. At the time, all 120 songs used in the experiment were by artists who were unsigned and not widely known. "The next day, in the lab, we talked about it."

To find out what had become of the songs, the lab bought a subscription to Nielsen SoundScan, a service that tracks music sales. The database contained sales data for 87 of the 120 songs (not surprisingly, many songs had languished in MySpace obscurity). Berns reexamined the functional magnetic resonance imaging scans his group had collected from 27 adolescents in 2007, looking for regions of the brain where neural activity during a 15-second clip of a song correlated with the subject's likeability ratings. Two regions stood out: the orbitofrontal cortex and the nucleus accumbens. "That was a good check that we were on the right track, because we knew from a ton of other studies that those regions are heavily linked to reward and anticipation," Berns says.

Next, the researchers looked to see whether the activity in either of these two brain regions, averaged across subjects for each song, correlated with the song's sales through May 2010. It did, Berns and co-author Sara Moore report in a paper in press at the Journal of Consumer Psychology. The correlations were statistically significant but modest. Activity in the nucleus accumbens, the best predictor of song sales, accounts for about 10% of the variance in sales, Berns says. "It's not a hit maker," he cautions.

Intriguingly, the brain scan data predicted commercial success better than the subjects' likeability ratings, which did not correlate with sales. "What is new and interesting about this study is that brain signals predict sales in a situation where the ratings of the participants don't," says John-Dylan Haynes of the Bernstein Center for Computational Neuroscience in Berlin. Although several recent studies have shown it's possible to predict consumer choices from brain activity, Haynes says, it hasn't been clear whether brain scans can reveal anything about people's product preferences that couldn't be gained by simply asking them. In this case, at least, it seems they can.

"This is a really cool result," says Brian Knutson, a cognitive neuroscientist at Stanford University in Palo Alto, California. Showing that brain activity in a small group of people can predict the buying behavior of a much larger group of people is a novel and provocative finding, he says. But how does it work, and why would brain activity be better than the subjects' ratings? Knutson suggests that activity in the nucleus accumbens may provide a more pure indication of how much people actually want something, unencumbered by economic and social considerations that might influence their ratings—for example, whether one's credibility as a hard-rocking heavy metal fan would be undermined by a fondness for, well, Apologize.

There have been many dubious claims about "neuromarketing" strategies for using brain activity to assess consumer sentiment, says Antonio Rangel, a neuroeconomist at the California Institute of Technology in Pasadena. He sees the new study as an exciting proof of principle that in some cases neuroimaging can provide useful information not picked up by traditional methods such as consumer surveys and focus groups. Still, Rangel says, it's a long way from being a viable marketing tool. "I would not invest in a company based on this."

Scientists find gene vital to nerve cell development

2011-06-10T06:44:00.000-07:00

Scientists find gene vital to nerve cell development
June 9th, 2011 in Medicine & Health / Genetics

In healthy mice, individual Schwann cells wrap their membranes around a nerve cell’s axon many times. A cross-section of the resulting myelin sheath is visible as a thick band surrounding the axon in the “Normal” image on the left. In mice with a mutation in Gpr126, Schwann cells cannot make myelin and no thick layer surrounding axons is visible in the “Mutant” image on the right. KELLY R. MONK

The body’s ability to perform simple tasks like flex muscles or feel heat, cold and pain depends, in large part, on myelin, an insulating layer of fats and proteins that speeds the propagation of nerve cell signals.

Now, scientists have identified a gene in mice that controls whether certain cells in the peripheral nervous system can make myelin. Called Gpr126, the gene encodes a cellular receptor that could play a role in diseases affecting peripheral nerves, says Kelly R. Monk, PhD, assistant professor of developmental biology at Washington University School of Medicine in St. Louis.

“Researchers knew Gpr126 existed in humans, but no one knew what it did,” says Monk, who did this work while a postdoctoral researcher at Stanford University. “For 30 years or so, scientists have been looking for a cell receptor that controls myelination by raising levels of an important chemical messenger. We found it in zebrafish. And now we’ve shown that it’s present in mammals. It’s the first known function for this receptor, and it solved a decades-old mystery, which is exciting.”

The work is currently available online and will be published in the July 1 issue of the journal Development.

In a paper published in Science in 2009, Monk and her colleagues first showed that zebrafish require Gpr126 to make myelin in their peripheral nerves, but not in the brain or spinal cord of the central nervous system.

When a gene works a certain way in zebrafish, it likely works that way in mammals, according to William S. Talbot, PhD, professor of developmental biology at Stanford University and Monk’s postdoctoral advisor.

“The brain and spinal cord are fine in mice without the Gpr126 gene,” Talbot says. “But there is no myelin in the peripheral nerves, very much like in zebrafish. This is evidence that Gpr126 probably has a general role in myelin formation and nerve development in all vertebrates, including humans.”

The missing gene appears to disrupt specialized cells in the peripheral nervous system called Schwann cells, stopping those cells from enveloping and providing nutrients to the axons of nerves. Healthy Schwann cells wrap their membranes around nerve cell axons many times to form the myelin sheath that speeds the transmission of nerve cell signals.

In zebrafish without Gpr126, Schwann cells appear to develop and arrange themselves with individual axons normally at first. But when it comes time to wrap around the axon and make myelin, they stop short.

“From zebrafish, we thought this gene controlled only one very specific step of Schwann cell development,” Monk says. “But in mice the story is more complex.”

In mice without the gene, problems begin much earlier. The Schwann cells take longer to associate with individual axons and, compared to normal mice, there are many fewer axons. Such evidence leads Monk to speculate that the delayed sorting and failure of Schwann cells to wrap around axons causes the associated neurons to die. Because of these and other problems seen in mice without Gpr126 (including defects in the lungs, kidneys and cardiovascular system), Monk proposes that it plays more diverse roles in mice than in zebrafish. Although mice without Gpr126 never lived beyond two weeks, zebrafish with the same mutation survived to reproduce.

Because of its clear role in forming myelin, Gpr126 could be a possible target for therapies to treat peripheral neuropathies, common conditions where peripheral nerves are damaged. Such damage causes an array of problems including pain and numbness in the hands and feet, muscle weakness and even problems involving functions of internal organs such as digestion. Some peripheral neuropathies are genetic, but many result from diseases of aging and poor health, including complications from diabetes or side effects of chemotherapy.

With these conditions in mind, Monk and Talbot point out that Gpr126 is a member of a large family of cell surface receptors that are common targets for most commercially available drugs, treating conditions as diverse as allergies, ulcers and schizophrenia.

“We don’t know yet whether Gpr126 itself can be a drug target. But the fact that its relatives can,” Talbot says, “makes it especially interesting.”

Ongoing work in Monk’s lab seeks to further define the many roles of Gpr126 in mammals, including whether it could help direct Schwann cells to repair or regrow damaged myelin.

More information: Monk KR, Oshima K, Jors S, Heller S, Talbot WS. Gpr126 is essential for peripheral nerve development and myelination in mammals. Development. 138(13). July 2011.

Monk et al. A G protein-coupled receptor is essential for Schwann cells to initiate myelination. Science. 325. Sept. 2009.

Provided by Washington University School of Medicine in St. Louis

Attention and awareness aren't the same

2011-06-07T05:56:00.000-07:00

Attention and awareness aren't the same
June 6th, 2011 in Psychology & Psychiatry

Paying attention to something and being aware of it seems like the same thing -they both involve somehow knowing the thing is there. However, a new study, which will be published in an upcoming issue of Psychological Science, a journal of the Association for Psychological Science, finds that these are actually separate; your brain can pay attention to something without you being aware that it's there.

"We wanted to ask, can things attract your attention even when you don't see them at all?" says Po-Jang Hsieh, of Duke-NUS Graduate Medical School in Singapore and MIT. He co-wrote the study with Jaron T. Colas and Nancy Kanwisher of MIT. Usually, when people pay attention to something, they also become aware of it; in fact, many psychologists assume these two concepts are inextricably linked. But more evidence has suggested that's not the case.

To test this, Hsieh and his colleagues came up with an experiment that used the phenomenon called "visual pop-out." They set each participant up with a display that showed a different video to each eye. One eye was shown colorful, shifting patterns; all awareness went to that eye, because that's the way the brain works. The other eye was shown a pattern of shapes that didn't move. Most were green, but one was red. Then subjects were tested to see what part of the screen their attention had gone to. The researchers found that people's attention went to that red shape – even though they had no idea they'd seen it at all.

In another experiment, the researchers found that if people were distracted with a demanding task, the red shape didn't attract attention unconsciously anymore. So people need a little brain power to pay attention to something even if they aren't aware of it, Hsieh and his colleagues concluded.

Hsieh suggests that this could have evolved as a survival mechanism. It might have been useful for an early human to be able to notice and process something unusual on the savanna without even being aware of it, for example. "We need to be able to direct attention to objects of potential interest even before we have become aware of those objects," he says.

Provided by Association for Psychological Science

Examining the brain as a neural information super-highway

2011-06-03T05:33:00.000-07:00

Examining the brain as a neural information super-highway
June 2nd, 2011 in Neuroscience

An article demonstrating how tools for modeling traffic on the Internet and telephone systems can be used to study information flow in brain networks will be published in the open-access journal PLoS Computational Biology on 2nd June 2011.

The brain functions as a complex system of regions that must communicate with each other to enable everyday activities such as perception and cognition. This need for networked computation is a challenge common to multiple types of communication systems. Thus, important questions about how information is routed and emitted from individual brain regions may be addressed by drawing parallels with other well-known types of communication systems, such as the Internet.

The authors, from the Rotman Research Institute at Baycrest Centre, Toronto, Canada, showed that – similar to other communication networks – the timing pattern of information emission is highly indicative of information traffic flow through the network. In this study the output of information was sensitive to subtle differences between individual subjects, cognitive states and brain regions.

The researchers recorded electrical activity from the brain and used signal processing techniques to precisely determine exactly when units of information get emitted from different regions. They then showed that the times between successive departures are distributed according to a specific distribution. For instance, when research study participants were asked to open their eyes in order to allow visual input, emission times became significantly more variable in parts of the brain responsible for visual processing, reflecting and indicating increased neural "traffic" through the underlying brain regions.

This method can be broadly applied in neuroscience and may potentially be used to study the effects of neural development and aging, as well as neurodegenerative disease, where traffic flow would be compromised by the loss of certain nodes or disintegration of pathways.

More information: Mišić B, Vakorin VA, Kovačević N, Paus T, McIntosh AR (2011) Extracting Message Inter-Departure Time Distributions from the Human Electroencephalogram. PLoS Comput Biol 7(6): e1002065. doi:10.1371/journal.pcbi.1002065

Provided by Public Library of Science

Researchers map, measure brain's neural connections

2011-06-02T06:44:00.000-07:00

Researchers at Brown University have created a computer program to advance analysis of the neural connections in the human brain. The program's special features include a linked view for users to view both the 3-D image (top) and 2-D closeups of the neural bundles. Credit: Radu Jianu, Brown University

Medical imaging systems allow neurologists to summon 3-D color renditions of the brain at a moment's notice, yielding valuable insights. But sometimes there can be too much detail; important elements can go unnoticed.

The bundles of individual nerves that transmit information from one part of the brain to the other, like fiber-optic cables, are so intricate and so interwoven that they can be difficult to trace through standard imaging techniques. To help, computer science researchers at Brown University have produced 2-D maps of the neural circuitry in the human brain.

The goal is simplicity. The planar maps extract the neural bundles from the imaging data and present them in 2-D – a format familiar to medical professionals working with brain models. The Brown researchers also provide a web interface by integrating the neural maps into a geographical digital maps framework that professionals can use seamlessly to explore the data.

"In short, we have developed a new way to make 2-D diagrams that illustrate 3-D connectivity in human brains," said David Laidlaw, professor of computer science at Brown and corresponding author on the paper published in IEEE Transactions on Visualization and Computer Graphics. "You can see everything here that you can't really see with the bigger (3-D) images."

The 2-D neural maps are simplified representations of neural pathways in the brain. These representations are created using a medical imaging protocol that measures the water diffusion within and around nerves of the brain. The sheathing is composed of myelin, a fatty membrane that wraps around axons, the threadlike extensions of neurons that make up nerve fibers.

Medical investigators can use the 2-D neural maps to pinpoint spots where the myelin may be compromised, which could affect the vitality of the neural circuits. That can help identify pathologies, such as autism, that brain scientists increasingly believe manifest themselves in myelinated axons. Diseases associated with the loss of myelin affect more than 2 million people worldwide, according to the Myelin Project, an organization dedicated to advancing myelin-related research.

Researchers can use the 2-D neural maps to help identify whether the structure or the size of neural bundles differs among individuals and how any differences may relate to performance, skills or other traits. "It's an anatomical measure," Laidlaw said. "It's a tool that we hope will help the field."

While zeroing in on the brain's wiring, the team, including graduate students Radu Jianu and Çağatay Demiralp, added a "linked view" so users can toggle back and forth between the neural bundles in the 2-D image and the larger 3-D picture of the brain.

"What you see is what you operate," said Jianu, the paper's lead author. "There's no change in perspective with what you're working with on the screen."

Users can export the 2-D brain representations as images and display them in Web browsers using Google Maps. "The advantage of using this mode of distribution is that users don't have to download a large dataset, put it in the right format, and then use a complicated software to try and look at it, but can simply load a webpage," Jianu explained.

The program is designed to share research. Scientists can use the Web to review brain research in other labs that may be useful to their own work.

Provided by Brown University

Woman can literally feel the noise.

2011-05-31T05:53:00.001-07:00

Woman can literally feel the noise.

May 30th, 2011 in Neuroscience -- A case of a 36-year-old woman who began to literally 'feel' noise about a year and a half after suffering a stroke sparked a new research project by neuroscientist Tony Ro from the City College of New York and the Graduate Center of the City University. Research and imagery of the brain revealed that a link had grown between the woman’s auditory region and the somatosensory region, essentially connecting her hearing to her touch sensation.

Ro and his team presented the findings at the Acoustical Society of America’s meeting on May 25. They pointed out that both hearing and touch rely on vibrations and that this connection may be found in the rest of us as well.

Another researcher and neuroscientist Elizabeth Courtenay Wilson from Beth Israel Deaconess Medical Center in Boston agrees that there is a strong connection between the two. Her team believes that the ear evolved from skin in order to create a more finely tuned frequency analysis. She earned her PhD from MIT with a study on whether vibrations could help hearing aid performance. Her studies showed that individuals with normal hearing were better able to detect a weak sound when it was accompanied by a weak vibration to the skin.

Ro himself published another paper in Experimental Brain Research in 2009 focusing on what he calls the mosquito effect. Those pesky little bugs sound frequency makes our skin prickle and he believes that in order for this to work the frequency of sound must match the frequency of the vibrations we feel.

Functional MRI scans of the brain have revealed that the auditory region of the brain can become activated by a touch. It is believed by some researchers that areas of the brain that are designed to understand frequency may be responsible for this wire crossing, though they are not yet sure exactly where the two senses come together.

How our focus can silence the noisy world around us

2011-05-28T06:18:00.000-07:00

How our focus can silence the noisy world around us
May 27th, 2011 in Psychology & Psychiatry

How can someone with perfectly normal hearing become deaf to the world around them when their mind is on something else? New research funded by the Wellcome Trust suggests that focusing heavily on a task results in the experience of deafness to perfectly audible sounds.

In a study published in the journal 'Attention, Perception, & Psychophysics', researchers at UCL (University College London) demonstrate for the first time this phenomenon, which they term 'inattentional deafness'.

"Inattentional deafness is a common everyday experience," explains Professor Nilli Lavie from the Institute of Cognitive Neuroscience at UCL. "For example, when engrossed in a good book or even a captivating newspaper article we may fail to hear the train driver's announcement and miss our stop, or if we're texting whilst walking, we may fail to hear a car approaching and attempt to cross the road without looking."

Professor Lavie and her PhD student James Macdonald devised a series of experiments designed to test for inattentional deafness. In these experiments, over a hundred participants performed tasks on a computer involving a series of cross shapes. Some tasks were easy, asking the participants to distinguish a clear colour difference between the cross arms. Others were much more difficult, involving distinguishing subtle length differences between the cross arms.

Participants wore headphones whilst carrying out the tasks and were told these were to aid their concentration. At some point during task performance a tone was played unexpectedly through the headphones. At this point, immediately after the sound was played, the experiment was stopped and the participants asked if they had heard this sound.

When judging the respective colours of the arms - an easy task that takes relatively little concentration - around two in ten participants missed the tone. However, when focusing on the more difficult task - identifying which of the two arms was the longest - eight out of ten participants failed to notice the tone.

The researchers believe this deafness when attention is fully taken by a purely visual task is the result of our senses of seeing and hearing sharing a limited processing capacity. It is already known that people similarly experience 'inattentional blindness' when engrossed in a task that takes up all of their attentional capacity - for example, the famous Invisible Gorilla Test, where observers engrossed in a basketball game fail to observe a man in a gorilla suit walk past. The new research now shows that being engrossed in a difficult task makes us blind and deaf to other sources of information.

"Hearing is often thought to have evolved as an early warning system that does not depend on attention, yet our work shows that if our attention is taken elsewhere, we can be effectively deaf to the world around us," explains Professor Lavie. "In our task, most people noticed the sound if the task being performed was easy and did not demand their full concentration. However, when the task was harder they experienced deafness to the very same sound."

Other examples or real world situations include inattentional deafness whilst driving. It is well documented that a large number of accidents are caused by a driver's inattention and this new research suggests inattentional deafness is yet another contributing factor. For example, although emergency vehicle sirens are designed to be too loud to ignore, other sounds - such as a lorry beeping while reversing, a cyclist's bell or a scooter horn - may be missed by a driver focusing intently on some interesting visual information such as a roadside billboard, the advert content on the back of the bus in front or the map on a sat nav.

New imaging method identifies specific mental states

2011-05-27T07:31:00.000-07:00

New imaging method identifies specific mental states
May 26th, 2011 in Neuroscience

New clues to the mystery of brain function, obtained through research by scientists at the Stanford University School of Medicine, suggest that distinct mental states can be distinguished based on unique patterns of activity in coordinated "networks" within the brain. These networks consist of brain regions that are synchronously communicating with one another. The Stanford team is using this network approach to develop diagnostic tests in Alzheimer's disease and other brain disorders in which network function is disrupted.

In a novel set of experiments, a team of researchers led by Michael Greicius, MD, assistant professor of neurology and neurological sciences, was able to determine from brain-imaging data whether experimental subjects were recalling events of the day, singing silently to themselves, performing mental arithmetic or merely relaxing. In the study, subjects engaged in these mental activities at their own natural pace, rather than in a controlled, precisely timed fashion as is typically required in experiments involving the brain-imaging technique called functional magnetic resonance imaging. This suggests that the new method — a variation on the fMRI procedure — could help scientists learn more about what the brain is doing during the free-flowing mental states through which individuals move, minute-to-minute, in the real world.

FMRI can pinpoint active brain regions in which nerve cells are firing rapidly. In standard fMRI studies, subjects perform assigned mental tasks on cue in a highly controlled environment. The researcher typically divides the scan into task periods and non-task periods with strict start and stop points for each. Researchers can detect brain regions activated by the task by subtracting signals obtained during non-task periods from those obtained during the task. To identify which part of the brain is involved in, for example, a memory task, traditional fMRI studies require experimenters to control the timing of each recalled event.

"With standard fMRI, you need to know just when your subjects start focusing on a mental task and just when they stop," said Greicius. "But that isn't how real people in the day-to-day world think."

In their analysis, the Stanford team broke free of this scripted approach by looking not for brain regions that showed heightened activity during one mental state versus another, but for coordinated activity between brain regions, defining distinct brain states. This let subjects think in a self-paced manner more closely resembling the way they think in the world outside the MRI scanner. Instead of breaking up a cognitive state into short blocks of task and non-task, Greicius and his team used uninterrupted scan periods ranging from 30 seconds to 10 minutes in length, allowing subjects to follow their own thought cues at their own pace. The scientists were able to accurately capture subjects' mental states even when the duration of the scans was reduced to as little as one minute or less — all the more reflective of real-world cognition.

Greicius is senior author of the new study, to be published online May 26 in Cerebral Cortex. His team obtained images from a group of 14 young men and women who underwent four 10-minute fMRI scans apiece. Importantly, during each of the four scans, the investigators didn't tell subjects exactly when to start doing something — recall events, sing to themselves silently, count back from 5,000 by threes, or just rest — or when to switch to something else, as is typical with standard fMRI research. "We just told them to go at their own pace," Greicius said.

Greicius's team assembled images from each separate scan. Instead of comparing "on-task" images with "off-task" images to see which regions were active during a distinct brain state compared with when the brain wasn't in that state, the researchers focused on which collections, or networks, of brain regions were active in concert with one another throughout a given state.

Greicius and his colleagues have previously shown that the brain operates, at least to some extent, as a composite of separate networks composed a number of distinct but simultaneously active brain regions. They have identified approximately 15 such networks. Different networks are associated with vision, hearing, language, memory, decision-making, emotion and so forth.

>From the scans of those 14 healthy volunteers, the Stanford investigators were able to construct maps of coordinated activity in the brain during each of the four mental activities. In particular, they looked at 90 brain regions distributed across multiple networks, accounting for most of the brain's gray matter.

In their analysis, the Stanford team identified groups of regions throughout the brain whose activity was correlated to form functional networks. The new fMRI method let them view such networks within a single scan, without having to compare it to another scan via subtraction. In the scanning images, different thought processes showed up as different networks or regions communicating with one another. For example, subjects' recollection of the day's events was characterized by synchronous firing of two brain regions called the retrosplenial cortex, or RSC, and medial temporal lobe, or MTL. Standard fMRI, in which the brain's activity during a recall exercise was compared to its activity in the resting state, has already shown that the RSC and MTL are each active during memory-related tasks. But the new study showed that coordinated activity between these two regions indicates that subjects were engaged in recall.

Once they had completed their mapping of the four mental states to specific patterns of connectivity across the 90 brain regions, Greicius and his colleagues tested their ability to determine which state a subject was in by asking a second group of 10 subjects to undergo scanning during the same four mental activities. By comparing the pattern of a subject's image to the patterns assigned to each of the four states from the 14-subject data set, the researchers' analytical tools were, with 85 percent accuracy, able to correctly determine which mental state a particular scanning image corresponded to. The team's ability to correctly determine which of those four mental tasks a subject was performing remained at the 80 percent accuracy level even when scanning sessions were reduced to one minute apiece — a length of time more reflective of real-life mental behavior than the customary 10-minute scanning time.

As an additional test, Greicius's team asked the second participant group to engage in a fifth cognitive activity, spatial navigation, in which subjects were asked to imagine walking through the rooms of their home. The team's analytical tools readily rejected the connectivity pattern reflecting this mental activity as not indicative of one of the four states in question.

The ability to use fMRI in a more casual, true-to-life manner for capturing the mental states of normal volunteers bodes well for assessing patients with cognitive disorders, such as people with Alzheimer's disease or other dementias, who are often unable to follow the precise instructions and timing demands required in traditional fMRI.

In fact, the technique has already begun proving its value in diagnosing brain disorders. In a 2009 study in Neuron, Greicius and his associates showed that different cognitive disorders show up in fMRI scans as having deficiencies specific to different networks. In Alzheimer's disease, for example, the network associated with memory is functionally impaired so that its component brain regions are no longer firing in a coordinated fashion. This network approach to brain function and dysfunction is now being widely applied to the study of numerous neurological and psychiatric conditions.

Provided by Stanford University Medical Center

Brain cell networks recreated with new view of activity behind memory formation

2011-05-26T09:29:00.000-07:00

A fluorescent image of the neural network model developed at Pitt reveals the interconnection (red) between individual brain cells (blue). Adhesive proteins (green) allow the network to be constructed on silicon discs for experimentation. Credit: U. Pittsburgh

University of Pittsburgh researchers have reproduced the brain's complex electrical impulses onto models made of living brain cells that provide an unprecedented view of the neuron activity behind memory formation.

The team fashioned ring-shaped networks of brain cells that were not only capable of transmitting an electrical impulse, but also remained in a state of persistent activity associated with memory formation, said lead researcher Henry Zeringue [zuh-rang], a bioengineering professor in Pitt's Swanson School of Engineering. Magnetic resonance images have suggested that working memories are formed when the cortex, or outer layer of the brain, launches into extended electrical activity after the initial stimulus, Zeringue explained. But the brain's complex structure and the diminutive scale of neural networks mean that observing this activity in real time can be nearly impossible, he added.

The Pitt team, however, was able to generate and prolong this excited state in groups of 40 to 60 brain cells harvested from the hippocampus of rats—the part of the brain associated with memory formation. In addition, the researchers produced the networks on glass slides that allowed them to observe the cells' interplay. The work was conducted in Zeringue's lab by Pitt bioengineering doctoral student Ashwin Vishwanathan, who most recently reported the work in the Royal Society of Chemistry (UK) journal, Lab on a Chip. Vishwanathan coauthored the paper with Zeringue and Guo-Qiang Bi, a neurobiology professor in Pitt's School of Medicine. The work was conducted through the Center for the Neural Basis of Cognition, which is jointly operated by Pitt and Carnegie Mellon University.

To produce the models, the Pitt team stamped adhesive proteins onto silicon discs. Once the proteins were cultured and dried, cultured hippocampus cells from embryonic rats were fused to the proteins and then given time to grow and connect to form a natural network. The researchers disabled the cells' inhibitory response and then excited the neurons with an electrical pulse.

Zeringue and his colleagues were able to sustain the resulting burst of network activity for up to what in neuronal time is 12 long seconds. Compared to the natural duration of .25 seconds at most, the model's 12 seconds permitted an extensive observation of how the neurons transmitted and held the electrical charge, Zeringue said.

Unraveling the mechanics of this network communication is key to understanding the cellular and molecular basis of memory creation, Zeringue said. The format developed at Pitt makes neural networks more accessible for experimentation. For instance, the team found that when activity in one neuron is suppressed, the others respond with greater excitement.

"We can look at neurons as individuals, but that doesn't reveal a lot," Zeringue said. "Neurons are more connected and interdependent than any other cell in the body. Just because we know how one neuron reacts to something, a whole network can react not only differently, but sometimes in the complete opposite manner predicted."

Zeringue will next work to understand the underlying factors that govern network communication and stimulation, such as the various electrical pathways between cells and the genetic makeup of individual cells.

Provided by University of Pittsburgh

Eggs, butter, milk -- memory is not just a shopping list

2011-05-24T07:04:00.001-07:00

Eggs, butter, milk -- memory is not just a shopping list
May 23rd, 2011 in Psychology & Psychiatry

Often, the goal of science is to show that things are not what they seem to be. But now, in an article which will be published in an upcoming issue of Perspectives on Psychological Science, a journal of the Association for Psychological Science, a veteran cognitive psychologist exhorts his colleagues in memory research to consult the truth of their own experience.

"Cognitive psychologists are trying to be like physicists and chemists, which means doing controlled laboratory experiments, getting numbers out of them and explaining the numbers," says Douglas L. Hintzman, now retired from the University of Oregon. The lion's share of experiments, he says, involve giving people lists of words and asking them to remember the words.

"Researchers often completely forget that they have memories and they can see how their memories work from the inside," he continues, "—and that this may be very relevant to the theory they are developing."

Reviewing the literature in his field and the experimental models that have come in and gone out of fashion over the last half-century, Hintzman concludes that these simple experimental tasks, observed in isolation from one another, yield theories that are so oversimplified as to fundamentally misrepresent the nature of memory.

For instance, he says, these word-list tasks make it look as if we only remember when we intentionally put our minds to it— yet we all experience spontaneous memories, many times every day.

Also, because these experiments take place in short sessions, researchers ignore the obvious fact that memory is about personal history, and history is laid out in time. Memory, then, is basic to our understanding of time.

The preference for so-called theoretical parsimony—the idea that a theory should be no more complex than necessary—leads memory scientists up the wrong path, he writes: "The breadth of a theory is at least as important as its precision. Indeed, if we take the theory of evolution as our standard, breadth would appear to be far more important."

Contemplating evolution, Hintzman has come to believe that a crucial role is played by what he calls "involuntary reminding"—the process by which current experiences evoke memories of earlier experiences, creating a coherent record of our interactions with the environment.

"Animals—mammals in particular—evolved in a complex world in which patterns of related events are distributed over time. It's essential for survival that you learn about these patterns." Humans have developed the additional ability to learn and retrieve memories deliberately, he continues. But "the evolutionary purpose of memory is revealed" by these everyday remindings, "not by what typically goes on in the lab."

In this article, Hintzman does not outline a research program for the future, but urges memory researchers and theorists to consider the wide variety of things that memory does for us. "Our ancestors' survival," he writes, "did not hinge on their ability to remember shopping lists. Hunter-gatherers take what they can find."

Provided by Association for Psychological Science

Scientists cultivate human brain's most ubiquitous cell in lab dish

2011-05-22T21:31:00.000-07:00

Scientists cultivate human brain's most ubiquitous cell in lab dish
May 22nd, 2011 in Biology / Biotechnology
Astrocytes are star-shaped cells that are the most common cell in the human brain and have now been grown from embryonic and induced stem cells in the laboratory of UW-Madison neuroscientist Su-Chun Zhang. Once considered mere putty or glue in the brain, astrocytes are of growing interest to biomedical research as they appear to play key roles in many of the brain's basic functions, as well as neurological disorders ranging from headaches to dementia. In this picture astrocyte progenitors and immature astrocytes cluster to form an "astrosphere." Photo provided by Robert Krencik/ UW-Madison
Pity the lowly astrocyte, the most common cell in the human nervous system.

Long considered to be little more than putty in the brain and spinal cord, the star-shaped astrocyte has found new respect among neuroscientists who have begun to recognize its many functions in the brain, not to mention its role in a range of disorders of the central nervous system.

Now, writing in the current (May 22) issue of the journal Nature Biotechnology, a group led by University of Wisconsin-Madison stem cell researcher Su-Chun Zhang reports it has been able to direct embryonic and induced human stem cells to become astrocytes in the lab dish.

The ability to make large, uniform batches of astrocytes, explains Zhang, opens a new avenue to more fully understanding the functional roles of the brain's most commonplace cell, as well as its involvement in a host of central nervous system disorders ranging from headaches to dementia. What's more, the ability to culture the cells gives researchers a powerful tool to devise new therapies and drugs for neurological disorders.

"Not a lot of attention has been paid to these cells because human astrocytes have been hard to get," says Zhang, a researcher at UW-Madison's Waisman Center and a professor of neuroscience in the UW-Madison School of Medicine and Public Health. "But we can make billions or trillions of them from a single stem cell."

Although astrocytes have gotten short shrift from science compared to neurons, the large filamentous cells that process and transmit information, scientists are turning their attention to the more common cells as their roles in the brain become better understood. There are a variety of astrocyte cell types and they perform such basic housekeeping tasks as helping to regulate blood flow, soaking up excess chemicals produced by interacting neurons and controlling the blood-brain barrier, a protective filter that keeps dangerous molecules from entering the brain.

Astrocytes, some studies suggest, may even play a role in human intelligence given that their volume is much greater in the human brain than any other species of animal.

"Without the astrocyte, neurons can't function," Zhang notes. "Astrocytes wrap around nerve cells to protect them and keep them healthy. They participate in virtually every function or disorder of the brain."

The ability to forge astrocytes in the lab has several potential practical outcomes, according to Zhang. They could be used as screens to identify new drugs for treating diseases of the brain, they can be used to model disease in the lab dish and, in the more distant future, it may be possible to transplant the cells to treat a variety of neurological conditions, including brain trauma, Parkinson's disease and spinal cord injury. It is possible that astrocytes prepared for clinical use could be among the first cells transplanted to intervene in a neurological condition as the motor neurons affected by the fatal amyotrophic lateral sclerosis, also known as Lou Gehrig's disease, are swathed in astrocytes.

"With an injury or neurological condition, neurons in the brain have to work harder, and doing so they make more neurotransmitters," chemicals that in excess can be toxic to other cells in the brain, Zhang says.

"One idea is that it may be possible to rescue motor neurons by putting normal, healthy astrocytes in the brain," according to Zhang. "These cells are really useful as a therapeutic target."

The technology developed by the Wisconsin group lays a foundation to make all the different species of astrocytes. What's more, it is possible to genetically engineer them to mimic disease so that previously inaccessible neurological conditions can be studied in the lab.

Provided by University of Wisconsin-Madison

'Mind reading' brain scans reveal secrets of human vision

2011-05-20T07:47:00.000-07:00

'Mind reading' brain scans reveal secrets of human vision
May 19th, 2011 in Neuroscience

Researchers were able to determine that study participants were looking at this street scene even when the participants were only looking at the outline. Credit: Fei-Fei Li

Researchers call it mind reading. One at a time, they show a volunteer – who's resting in an MRI scanner – a series of photos of beaches, city streets, forests, highways, mountains and offices. The subject looks at the photos, but says nothing.

The researchers, however, can usually tell which photo the volunteer is watching at any given moment, aided by sophisticated software that interprets the signals coming from the scan. They glean clues not only by noting what part of the brain is especially active, but also by analyzing the patterns created by the firing neurons. They call it decoding.

Now, psychologists and computer scientists at Stanford, Ohio State University and the University of Illinois at Urbana–Champaign have taken mind reading a step further, with potential impact on how both computers and the visually impaired make sense of the world they see.

The researchers, including Stanford computer scientist Fei-Fei Li, removed almost all of the detail from the color photographs, leaving only sparse line drawings of the assorted scenes. When they ran the experiment again with just the outlines, the researchers were still able to read the minds of the participants – with as much accuracy as before.

The research was focused on the parahippocampal place area, a region of the brain that plays an important role in recognition of scenes such as rooms, landscapes and city streets.

The results demonstrate that outlines play a crucial role in how the human eye and mind interpret what is seen. The bare outlines of the photos shown to the participants seemingly offered the brain almost as many clues as the original photo. This "impoverished" signal sent to the brain was enough, Li said.

The significance of the work? "By noting what is driving the brain, you will be learning the way the brain works," Li said, "why certain cues are more important than other cues."

"Mind reading" could prove helpful in assessing patients in comas. "Inferring what people are seeing is clinically important," Li said.

The drawing of a dog as part of the Nazca Lines geoglyphs, Peru, ca. 700-200 B.C. suggests the power of outlines throughout time.

Credit: Steve Taylor / Creative Commons

The power of outlines seems backed up by history and common experience. As the authors wrote in their research paper, published in the Proceedings of the National Academy of Sciences, early cave dwellers drew outline figures on the walls of their homes; Chinese calligraphy revolves around lines and strokes; and children draw outlines as they attempt to describe the world unfolding before them.

"The representations in our brain for categorizing these scenes seem to be a bit more abstract than some may have thought – we don't need features such as texture and color to tell a beach from a street scene," said Dirk Bernhardt-Walther, a psychologist at Ohio State University who was a member of the research team.

Even when the software made errors reading the black-and-white line drawing of, for example, the beach, the mistakes closely resembled the mistakes made with the color photo of the beach, underscoring the conclusion that line drawings stimulate the mind in almost the same way as color photographs.

As researchers began removing parts of the line drawings piece by piece before showing them to the participants, they learned that the longer contours created by the lines, which formed the structure of the scene, were the most important.

"Lines capture really important structure, and you can find evidence of that in the brain," Li said.

Provided by Stanford University

The odds are against extra-sensory perception

2011-05-19T08:19:00.000-07:00

The odds are against extra-sensory perception
May 18th, 2011 in Psychology & Psychiatry

Can people truly feel the future? Researchers remain skeptical, according to a new study by Jeffrey Rouder and Richard Morey from the University of Missouri in the US, and the University of Groningen in the Netherlands, respectively. Their work appears online in the Psychonomic Bulletin & Review, published by Springer.

Although extra-sensory perception (ESP) seems impossible given our current scientific knowledge, and certainly runs counter to our everyday experience, a leading psychologist, Daryl Bem of Cornell University, is claiming evidence for ESP. Rouder and Morey look at the strength of the evidence in Dr. Bem's experiments.

Their application of a relatively new statistical method that quantifies how beliefs should change in light of data, suggests that there is only modest evidence behind Dr. Bem's findings (that people can feel, or sense, salient events in the future that could not otherwise be anticipated, and cannot be explained by chance alone), certainly not enough to sway the beliefs of a skeptic.

They highlight the limitations of conventional statistical significance testing (p values), and apply a new technique (meta-analytical Bayes factor) to Dr. Bem's data, which overcomes some of these limitations. According to Rouder and Morey, in order to accurately assess the total evidence in Bem's data, it is necessary to combine the evidence across several of his experiments, not look at each one in isolation, which is what researchers have done up till now. They find there is some evidence for ESP – people should update their beliefs by a factor of 40.

In other words, beliefs are odds. For example, a skeptic might hold odds that ESP is a long shot at a million-to-one, while a believer might believe it is as possible as not (one-to-one odds). Whatever one's beliefs, Rouder and Morey show that Bem's experiments indicate they should change by a factor of 40 in favor of ESP. The believer should now be 40-to-1 sure of ESP, while the skeptic should be 25000-to-1 sure against it.

Rouder and Morey conclude that the skeptics odds are appropriate: "We remain unconvinced of the viability of ESP. There is no plausible mechanism for it, and it seems contradicted by well-substantiated theories in both physics and biology. Against this background, a change in odds of 40 is negligible."

More information: Rouder JN & Morey RD (2011). A Bayes factor meta-analysis of Bem's ESP claim. Psychonomic Bulletin & Review. DOI 10.3758/s13423-011-0088-7

Tiny variation in one gene may have led to crucial changes in human brain

2011-05-15T22:15:00.000-07:00

Tiny variation in one gene may have led to crucial changes in human brain
May 15th, 2011 in Genetics

On the left, the occipital region of a normal human brain is circled. On the right, the same area of the brain of a subject with mutation of LAMC3 gene is smooth, and lacks normal folds and convolutions. Credit: courtesy of Yale University

The human brain has yet to explain the origin of one its defining features – the deep fissures and convolutions that increase its surface area and allow for rational and abstract thoughts.

An international collaboration of scientists from the Yale School of Medicine and Turkey may have discovered humanity's beneficiary – a tiny variation within a single gene that determines the formation of brain convolutions – they report online May 15 in the journal Nature Genetics.

A genetic analysis of a Turkish patient whose brain lacks the characteristic convolutions in part of his cerebral cortex revealed that the deformity was caused by the deletion of two genetic letters from 3 billion in the human genetic alphabet. Similar variations of the same gene, called laminin gamma3 (LAMC3), were discovered in two other patients with similar abnormalities.

"The demonstration of the fundamental role of this gene in human brain development affords us a step closer to solve the mystery of the crown jewel of creation, the cerebral cortex," said Murat Gunel, senior author of the paper and the Nixdorff-German Professor of Neurosurgery, co-director of the Neurogenetics Program and professor of genetics and neurobiology at Yale.

The folding of the brain is seen only in mammals with larger brains, such as dolphins and apes, and is most pronounced in humans. These fissures expand the surface area of the cerebral cortex and allow for complex thought and reasoning without taking up more space in the skull. Such foldings aren't seen in mammals such as rodents or other animals. Despite the importance of these foldings, no one has been able to explain how the brain manages to create them. The LAMC3 gene – involved in cell adhesion that plays a key role in embryonic development – may be crucial to the process.

An analysis of the gene shows that it is expressed during the embryonic period that is vital to the formation of dendrites, which form synapses or connections between brain cells. "Although the same gene is present in lower organisms with smooth brains such as mice, somehow over time, it has evolved to gain novel functions that are fundamental for human occipital cortex formation and its mutation leads to the loss of surface convolutions, a hallmark of the human brain," Gunel said.

Provided by Yale University

Red dots signal the location of electrical impulses generated within this grid cell, which are needed for the brain to store information about the rat

2011-04-29T05:17:00.000-07:00

Red dots signal the location of electrical impulses generated within this grid cell, which are needed for the brain to store information about the rat's physical environment.

Biologists at UC San Diego have discovered that electrical oscillations in the brain, long thought to play a role in organizing cognitive functions such as memory, are critically important for the brain to store the information that allows us to navigate through our physical environment.

The scientists report in the April 29 issue of the journal Science that neurons called "grid cells" that create maps of the external environment in one portion of our brain require precisely timed electrical oscillations in order to function properly from another part of the brain that serves as a kind of neural pacemaker.

Their discovery has important implications for understanding the underlying causes of neurological diseases such as Alzheimer's disease and for restoring memory in areas of the brain that are necessary for orientation.

"This work is the first to demonstrate that oscillatory activity has a well-defined function in brain areas that store memories," says Stefan Leutgeb, an assistant professor of biology at UCSD who headed the team of researchers.

Scientists have long known that among the first brain areas to degenerate in Alzheimer's disease, leading to symptoms such as memory loss and disorientation, are the hippocampus and the nearby entorhinal cortex, important structures for the formation of memory. Those two regions of the brain contain three types of neurons that contribute to the formation of spatial memories and the spatial information in episodic memories from our life experiences.

These three types of neurons provide an internal GPS system to the brain. For example, one type of neuron, called "place cells," generates electrical activity only when an animal is at a certain position, while another type, called "head direction cells," acts like a compass. A third class of neurons, called "grid cells," provides grid-like patterns for the brain to store memories of physical dimensions of the external environment. The most striking feature about these cells is that their electrical activity is distributed at equidistant, periodic locations within each cell (shown in the figure). Grid cells were discovered by Norwegian scientists in rats in 2005, but in 2010 researchers in London detected groups of cells in human entorhinal cortex that share the same characteristics.

Leutgeb and his team of UCSD biologists—postdoctoral researcher Julie Koenig, undergraduate student Ashley Linder and Jill Leutgeb, an assistant professor of biology—were motivated to understand the function of electrical oscillations in the brain, which are routinely measured in clinical settings to diagnose neurological disorders.

Leutgeb's group demonstrated that neurons called grid cells in the entorhinal cortex that create maps of the external environment require precisely timed electrical oscillatory input signals from a neural pacemaker in the subcortex of the brain to function properly.

"Our findings represent a major milestone in understanding memory processing, and they will guide efforts to restore memory function when cells in the entorhinal cortex are damaged," says Stefan Leutgeb.

A group of scientists from Boston University reports related findings in a companion paper in the same April 29th issue of Science.

The UCSD researchers monitored the electrical activity of grid cells in rats that explored a small four-foot by four-foot enclosure. Grid cells, located in the entorhinal cortex just adjacent to the hippocampus, maintain an internal representation of the external environment. This representation is a grid-like map made of repeating equilateral triangles that tile the space in a hexagonal pattern. As an animal navigates through its environment, a given grid cell becomes active when the animal's position coincides with any of the vertices within the grid.

The scientists silenced the oscillatory input by manipulating a small group of pacemaker cells in the brain and observed a significant deterioration of the grid cells' maps of the environment.

Surprisingly, silencing the oscillatory input did not disrupt brain signals that indicate precise location (provided by place cells) and the compass signal (provided by head direction cells).

"It has been thought that the hippocampus is under control of the entorhinal cortex, so there was the assumption that grid cells would have a very large impact on place cells. We are surprised at how the function of place cells is maintained in the face of significant disruption in grid cell function," says Leutgeb.

"This important result shows that, in general, you can eliminate a substantial amount of incoming information to a brain circuit without that brain circuit losing a majority of its functionality," he adds. "The implication of this finding is that restoring memory function does not require that we exactly reassemble damaged neural circuitry, rather we can regain function by preserving or restoring key components."

"Our findings are a major step towards identifying these key components in an effort to preserve memory function in aging individuals and in patients with neurodegenerative diseases," he says.

Provided by University of California - San Diego

Neurorobotics reveals brain mechanisms of self-consciousness

2011-04-28T05:18:00.000-07:00

Neurorobotics reveals brain mechanisms of self-consciousness
April 27th, 2011 in Neuroscience

A new study uses creative engineering to unravel brain mechanisms associated with one of the most fundamental subjective human feelings: self-consciousness. The research, published by Cell Press in the April 28 issue of the journal Neuron, identifies a brain region called the temporo-parietal junction (TPJ) as being critical for the feeling of being an entity localized at a particular position in space and for perceiving the world from this position and perspective.

Recent theories of self-consciousness highlight the importance of integrating many different sensory and motor signals, but it is not clear how this type of integration induces subjective states such as self-location ("Where am I in space?") and the first-person perspective ("From where do I perceive the world?"). Studies of neurological patients reporting out-of-body experiences have provided some evidence that brain damage interfering with the integration of multisensory body information may lead to pathological changes of the first-person perspective and self-location. However, it is still not known how to examine brain mechanisms associated with self-consciousness.

"Recent behavioral and physiological work, using video-projection and various visuo-tactile conflicts showed that self-location can be manipulated in healthy participants," explains senior study author, Dr. Olaf Blanke, from the Ecole Polytechnique Fédérale de Lausanne in Switzerland. "However, so far these experimental findings and techniques do not allow for the induction of changes in the first-person perspective and have not been integrated with neuroimaging, probably because the experimental set-ups require participants to sit, stand, or move. This makes it very difficult to apply and film the visuo-tactile conflicts on the participant's body during standard brain imaging techniques."

Making use of inventive neuroimaging-compatible robotic technology that was developed by Dr. Gassert's group at the Swiss Federal Institute of Technology in Zurich, Dr. Blanke and colleagues studied healthy subjects and employed specific bodily conflicts that induced changes in self-location and first-person perspective while simultaneously monitoring brain activity with functional magnetic resonance imaging. They observed that TPJ activity reflected experimental changes in self-location and first-person perspective. The researchers also completed a large study of neurological patients with out-of-body experiences and found that brain damage was localized to the TPJ.

"Our results illustrate the power of merging technologies from engineering with those of neuroimaging and cognitive science for the understanding of the nature of one of the greatest mysteries of the human mind: self-consciousness and its neural mechanisms," concludes Dr. Blanke. "Our findings on experimentally and pathologically induced altered states of self-consciousness present a powerful new research technology and reveal that TPJ activity reflects one of the most fundamental subjective feelings of humans: the feeling that 'I' am an entity that is localized at a position in space and that 'I' perceive the world from here."

More information: Ionta et al.: “Multisensory Mechanisms in Temporo-Parietal Cortex Support Self-Location and First-Person Perspective.”

Provided by Cell Press

"Neurorobotics reveals brain mechanisms of self-consciousness." April 27th, 2011. http://medicalxpress.com/news/2011-04-neurorobotics-reveals-brain-mechanisms-self-consciousness.html

New study examines brain processes behind facial recognition

2011-04-20T14:43:00.001-07:00

New study examines brain processes behind facial recognition
April 18th, 2011 in Medicine & Health / Neuroscience

When you think you see a face in the clouds or in the moon, you may wonder why it never seems to be upside down.

It turns out the answer to this seemingly minor detail is that your brain has been wired not to.

Using tests of visual perception and functional magnetic resonance imaging (fMRI), Lars Strother and colleagues at The University of Western Ontario's world-renowned Centre for Brain & Mind recently measured activity in two regions of the brain well known for facial recognition and found they were highly sensitive to the orientation of people's faces.

The team had participants look at faces that had been camouflaged and either held upright or turned upside down. They found that right-side up faces were easier to see – and activated the face areas in the brain more strongly – thus demonstrating that our brains are specialized to understand this orientation.

The surprise came when they found this bias in brain activity also applies to pictures of animals.

Like faces, animals are biological visual forms that have a typical upright orientation. In the study, published in the current issue of the journal PLoS ONE, Strother and his colleagues propose that the human visual system allows us to see familiar objects – not just faces – more easily when viewed in the familiar upright orientation.

They also demonstrated this bias can be found in the neural activity of those brain areas involved with the most basic steps in visual processing, when visual inputs from the eyes first reach the brain.

In future research, the team hopes to chase down how this bias is set up in these early visual areas of the brain – and what this tells us about how brain circuits can be modified by knowledge and experience.

Provided by University of Western Ontario

Skywalker ensures optimal communication between neurons

2011-04-02T08:56:00.000-07:00

Skywalker ensures optimal communication between neurons
April 1st, 2011 in Medicine & Health / Neuroscience

Patrik Verstreken (VIB/K.U.Leuven, Belgium) has discovered the mechanism that ensures neurons can continue to send the right signals for long consecutive periods - a process that is disrupted in neurological diseases such as Parkinson's. Verstreken and his colleagues discovered that an enzyme called Skywalker controls the subtle balance in communication.

"I hope that unraveling the way Skywalker works will not only teach us more about the way neurons communicate with each other but will also lead to new diagnostics and therapies for neurological diseases such as Parkinson's," says Verstreken.

Communication between brain cells

Brain disorders take a major toll on society. More than 8% of the population in the West depends on analgesics. Twenty per cent suffers from a mental disturbance and the number of people suffering from the effects of neurological diseases is estimated at 1 billion. Many of these problems are caused by the disruption of communication between brain cells. Hence, finding a solution depends on understanding this communication in the smallest details.

Communication between brain cells occurs at the synapses, where an electrical signal is passed via a vesicle (a small membrane-enclosed sac with signaling substances). The vesicle releases the signaling substances, thus activating another brain cell.

An eye for the proper balance

The vesicles are reused several times. This results in the gradual degradation of the proteins they need for carrying out their function properly, which in turn affects the release of signaling substances. How the vesicles are kept operational during this recycling process was a mystery until now. Most types of cells have incorporated an extra step into this recycling process via special cell compartments called endosomes. In the endosomes, vesicle proteins are sorted to ensure optimal functioning of the recycled vesicles.

However, it was not clear whether this extra step was relevant for vesicle recycling in brain cells. Various studies seemed to demonstrate that it was in fact missing in brain cells.

Skywalker regulates communication between brain cells

Patrik Verstreken and his colleagues have now discovered an enzyme, christened Skywalker, which regulates this extra step. The VIB researchers tested fruit flies unable to produce Skywalker. In these so-called sky flies, they noticed that broken-down proteins from the vesicles were more easily replaced, and that many more signaling substances were released than in the synapses of normal fruit flies. In other words, a lack of Skywalker increases the signal between two brain cells, resulting in overstressed flies.

But the discovery that inhibition of Skywalker leads to a stronger signal between brain cells offers possibilities for the fight against neurological diseases such as Parkinson's. In the early stages of these diseases, the signals between brain cells are too weak. Verstreken wants to study this further, but realizes that it will be an enormous challenge to find ways to maintain the subtle balance that ensures optimal communication.

More information: Loss of Skywalker reveals synaptic endosomes as sorting stations for synaptic vesicle proteins, Uytterhoeven et al., Cell.

Provided by Flanders Institute for Biotechnology

Brain scientists offer medical educators tips on the neurobiology of learning

2011-04-01T08:19:00.000-07:00

Brain scientists offer medical educators tips on the neurobiology of learning
March 30th, 2011 in Medicine & Health / Neuroscience

Everyone would like MDs to have the best education – and to absorb what they are taught. The lead article in the April 4 issue of the journal Academic Medicine* connects research on how the brain learns to how to incorporate this understanding into real world education, particularly the education of doctors.

"Repetition, reward, and visualization are tried and true teaching strategies. Now, knowing what is happening in the brain will enhance teaching and learning," said Michael J. Friedlander, executive director of the Virginia Tech Carilion Research Institute and professor of biological sciences and of biomedical engineering and science at Virginia Tech. He is the lead author on the article, "What can medical education learn from the neurobiology of learning?"

Friedlander collaborated on the article with Dr. Linda Andrews, senior associate dean for medical education, Baylor College of Medicine; Elizabeth G. Armstrong, director of Harvard Macy Institute, Harvard Medical School; Dr. Carol Aschenbrenner, executive vice president of the Association of American Medical Colleges; Dr. Joseph S. Kass, chief of neurology and director of the Stroke Center at Ben Taub Hospital and assistant professor of neurology, Center for Ethics and Health Policy, Baylor College of Medicine; Dr. Paul Ogden, associate dean for educational program development, Texas A&M Health Sciences Center and College of Medicine; Dr. Richard Schwartzstein, director of the Harvard Medical School Academy; and Dr. Tom Viggiano, the associate dean for faculty affairs, professor of medical education and medicine, and the Barbara Woodward Lips professor at Mayo Medical School.

The research

In the past 50 years, behavioral approaches combined with functional brain imaging and computational neuroscience have revealed strategies employed by mammals' brains to acquire, store, and retrieve information. In addition to molecular and cellular approaches to describe the workings of the underlying hardware changes that occur in the brain during learning and the formation of memories, there has also been progress in higher-order, human-based studies of cognition, including learning and memory. Scientists have used functional magnetic resonance imaging (fMRI) of the living brain combined with computational modeling to elucidate the strategies employed and the underlying biological processes.

The research has shown how learning leads to functional and structural changes in the cellular networks including the chemical communication points or synapses between neurons at a variety of sites throughout the central nervous system. The functional changes in the effectiveness of communication between individual neurons and within networks of neurons are accompanied by substantial changes in the structural circuitry of the brain, once thought to be hard-wired in adults.

"One of the most exciting advances, as a result of optical imaging of the living brain, is the demonstration that there is growth, retraction, and modifying connectivity between neurons," said Friedlander. "We have also seen that the mature brain can generate new neurons, although, this research is so new that the functional implications of these new neurons and their potential contribution to learning and memory formation remain to be determined," he said.

The recommendations

The most effective delivery of the best possible care requires identifying and assigning levels of importance to the biological components of learning. Here are 10 key aspects of learning based on decades of research by many scientists that the article's authors believe can be incorporated into effective teaching.

Repetition:
Medical curricula often employ compressed coverage over limited time frames of a great amount of material. Learning theory and the neurobiology of learning and memory suggest that going deeper is more likely to result in better retention and depth of understanding. With repetition, many components of the neural processes become more efficient, requiring less energy and leaving higher-order pathways available for additional cognitive processing. However, repetitions must be appropriately spaced.

Reward and reinforcement:
Reward is a key component of learning at all stages of life. "The brain's intrinsic reward system – self-congratulations with the realization of success -- plays a major role in reinforcement of learned behaviors," Friedlander said. "An important factor is the realization that accomplishing an immediate goal and a successful step toward a future goal can be equally rewarding."

In the case of medical students, there are considerable rewards ahead of them in addition to the more immediate rewards of the satisfaction of understanding medicine. The students who derive joy from learning as they proceed through their medical education may have a greater chance of using the brain's capacity to provide reward signals on an ongoing basis, facilitating their learning process.

Visualization:
Visualization and mental rehearsal are real biological processes with associated patterned activation of neural circuitry in sensory, motor, executive, and decision-making pathways in the brain. Internally generated activity in the brain from thoughts, visualization, memories, and emotions should be able to contribute to the learning process.

Active engagement:
There is considerable neurobiological evidence that functional changes in neural circuitry that are associated with learning occur best when the learner is actively engaged.. Learners' having multiple opportunities to assume the role of teacher also invoke neural motivation and reward pathways -- and another major biological component of the learning process: stress.

Stress:
Although the consequences of stress are generally considered undesirable, there is evidence that the molecular signals associated with stress can enhance synaptic activity involved in the formation of memory. However, particularly high levels of stress can have opposite effects. The small, interactive teaching format may be judiciously employed to moderately engage the stress system.

Fatigue:
Patterns of neuronal activity during sleep reinforce the day's events. Research suggests that it is important to have appropriate downtime between intense problem-solving sessions. Downtime permits consolidation away from the formal teaching process.

Multitasking:
Multitasking is a distraction from learning, unless all of the tasks are relevant to the material being taught. The challenge is to integrate information from multiple sources, such as a lecture and a hand-held device.

Individual learning styles:
Neural responses of different individuals vary, which is the rationale for embracing multiple learning styles to provide opportunities for all learners to be most effectively reached.

Active involvement:
Doing is learning. And success at doing and learning builds confidence.

Revisiting information and concepts using multimedia:
Addressing the same information using different sensory processes, such as seeing and hearing, enhances the learning process, potentially bringing more neural hardware to bear to process and store information.

The researchers recommend that medical students be taught the underlying neurobiological principles that shape their learning experiences. "By appealing not only to students' capacity to derive pleasure from learning about medicine but also to their intellectual capacity for understanding the rationale for the educational process selected … real motivation can be engendered. … They become more effective communicators and enhance their patients' success at learning the information they need for managing their own health and treatments as well."

More information: *"What Can Medical Education Learn From the Neurobiology of Learning?" by Michael J. Friedlander, PhD; Linda Andrews, MD; Elizabeth G. Armstrong, PhD; Carol Aschenbrenner, MD; Joseph S. Kass, MD; Paul Ogden, MD; Richard Schwartzstein, MD; and Thomas R. Viggiano, MD, MEd. Academic Medicine, Vol. 86, No. 4 / April 2011

Provided by Virginia Tech

Study shows some forms of visual reasoning might be inborn

2011-03-31T23:12:00.000-07:00

Study shows some forms of visual reasoning might be inborn
March 30th, 2011 in Medicine & Health / Research

Italian researcher Girogio Vallortigara of the University of Trento in Italy, and his colleagues have devised an experiment that shows that the ability to view and interpret what is normal and what is not, at least in vertebrates, might be imprinted on our brains before birth.

In a paper in Biology Letters, the researchers describe how they placed 66 baby chickens in a dark chamber immediately after birth to prevent them from forming any sort of visual reasoning abilities, then turned on the lights and presented them with two drawings; one of a cube with an M. C. Escher type staircase that could never exist in the real world as it wraps around the object in impossible ways, and the other a normal cube with a normal staircase. Two thirds of the chicks went for the real deal, while presumably the other third either did nothing, or tried out the impossible picture to see if they could climb those stairs and escape from their chamber after all.

The results show that the chicks do have some inborn ability to look at and recognize the difference between something that is visually possible and something that is not; and raises the issue of whether human beings have the same kind of skill. Human babies have been tested, and showed the same results, but not till they were four months old, and most certainly weren’t forced to live in the dark all that time, which meant they were able to build up their own ideas of what is real and what isn’t by existing and learning in a three dimensional world.

The study also lays open the question of how animals of any species come to understand what is possible and what isn’t in the world they inhabit. Other experiments have shown for example, that baby chicks won’t walk off the edge of a table, as they seemingly know they can’t fly; which begs the question, how did they come to know, and what causes them to change their minds as they grow older and their wings develop?

Once again, more research will be needed to find the ultimate answers to such difficult questions.

Could 'training the brain' help children with Tourette syndrome?

2011-03-25T08:33:00.000-07:00

Could 'training the brain' help children with Tourette syndrome?
March 24th, 2011 in Medicine & Health / Diseases

Children with Tourette syndrome could benefit from behavioural therapy to reduce their symptoms, according to a new brain imaging study.

Researchers at The University of Nottingham discovered that the brains of children with Tourette syndrome (TS) develop in a unique way — which could suggest new methods of treating the condition.

The study, published in the journal Current Biology, found that many children with TS experience a 'reorganisation' of the brain structure in their teens, as their brain compensates for the condition and allows them to gain control over their symptoms and tics.

Researchers believe that 'training' the brain to encourage this process — through the use of behavioural therapy — could help young people gain control over their symptoms more quickly and effectively. Effective behavioural therapies could involve habit reversal therapy.

The findings have significant implications because they suggest an alternative to drug-based therapies, which can have unwanted side-effects including weight gain and depression.

Study authors Professor Stephen Jackson and Professor Georgina Jackson used brain imaging and behavioural techniques to study a group of children with TS compared to a control group.

Stephen Jackson, Professor of Cognitive Neuroscience in the School of Psychology, said: "We had previously shown, somewhat paradoxically, that children with Tourette syndrome have greater control over their motor behaviour than typically-developing children of a similar age, and we had speculated that this was due to compensatory changes in the brain that helped these children control their tics.

"This new study provides compelling evidence that this enhanced control of motor output is accompanied by structural and functional alterations within the brain. This finding suggests that non-pharmacological, 'brain-training', approaches may prove to be an effective treatment for Tourette syndrome."

Tourette syndrome is an inherited neurological condition that affects one school child in every hundred. The key feature of TS is tics — involuntary and uncontrollable sounds and movements such as coughing, grunting, eye blinking and repeating of words.

Across the UK as a whole, TS affects more than 300,000 children and adults. The syndrome tends to be first identified around the ages of six to seven, with tics reaching their maximum level at the age of 12; for about half of children with TS, symptoms continue into adulthood.

Provided by University of Nottingham

Scientists identify neuron types that mediate different behavioral states

2011-03-18T08:14:00.000-07:00

Scientists identify neuron types that mediate different behavioral states
March 17th, 2011 in Medicine & Health / Neuroscience

In a recent study, scientists from the Max Planck Florida Institute have provided one of the most comprehensive analyses to date of the detailed architecture of individual functionally characterized neurons in the cerebral cortex, the largest and most complex area of the brain, whose functions include sensory perception, motor control, and cognition.

The study was published in the February edition of the Proceedings of the National Academy of Sciences (PNAS). This analysis provides complete three-dimensional reconstructions of the dendritic and axonal anatomy of individual neurons, identifies their target neurons throughout the sensory cortical area and describes the information relayed by these neurons during different behavioral states.

Mapping the connectivity within neuronal networks at the level of individual neurons is a major frontier in neuroscience and an essential step towards understanding how the brain works. “Neurons in the brain are grouped into different cell types, each cell type displaying characteristic anatomical and functional properties”, said Dr. Marcel Oberlaender, a scientist at the Max Planck Florida Institute and the first author of the study. “Identifying the three-dimensional pattern of the axon, the neurons’ ‘sending device’, is essential for defining the properties of neural circuits, and, more broadly, establishes the structural constraints that underlie the computational abilities of the brain.” The findings from this study could lead to a better understanding of how the cortex transforms sensory information into behavioral responses.

Reverse Engineering the Cerebral Cortex

The cerebral cortex is a thin sheet of neurons grouped into layers, which are arrayed parallel to the surface and columns that run perpendicular to the surface and span the depth of the cortex. The neurons within cortical columns share similar response properties and are considered a fundamental unit for processing sensory input. This study is part of a larger research program undertaken by scientists in the Digital Neuroanatomy research group at the Max Planck Florida Institute that aims to reverse engineer the three-dimensional structure and connectivity of neurons in cortical columns. They are focusing on a specialized set of columns in the cortex of the rat that processes sensory input from the facial whiskers, and where each separate whisker has its own specific column.

Dr. Oberlaender said that in related studies they identified nine different cell types and were able to quantify the number of neurons per type, their locations within the cortical column and their functional responses to two behavioral states, whisker motion and whisker touch, respectively. “Most interestingly,” Dr. Oberalender said, “two cell types, located in the same area of a cortical column were selectively active after whisker touch or during whisker motion.” The present study’s detailed three-dimensional reconstructions of the neurons’ ‘sending devices’ revealed that the two cell types also display distinct and characteristic axon projection patterns, providing strong evidence that cell type-specific cortical circuits mediate whisker motion and touch, respectively.

Reconstructing Neurons in Three Dimensions

The most challenging aspect of this new study was the quantitative approach taken by the scientists, an approach that involved the painstaking reconstruction of about 1 meter of axon from the two cell types, with axon diameters being usually smaller than 1 micron. To quantify the three-dimensional projection patterns of individual neurons, the scientists labeled each neuron in the living animal with a light-absorbing marker, which could then be viewed by advanced microscopy imaging techniques.

“We spent five years developing custom-designed imaging techniques and automated reconstruction and analysis tools,” admits Dr. Oberlaender, “because the axon of an individual neuron can innervate a volume of more than 10 cubic millimeters of the cerebral cortex and reaches total lengths of up to 10 centimeters. During the process, we generated terabytes of imaging data for each neuron, but we established a workflow that allows reconstructing such complex axonal structures from this large amount of data within less than a week.”

The result of all this advanced imaging and reconstruction analysis is a wealth of data on the cell type-specific architecture of the neuronal networks involved in whisker motion and touch, and enables the researches to hypothesize mechanisms that allow rodents to locate objects, and which will ultimately lead to understanding more complex behaviors, such as decision making.

“By integrating this new anatomical data into the reverse engineered model of a cortical column in rodent somatosensory cortex, we hope to be able to perform simulation experiments, which will potentially unravel cellular and network mechanisms that underlie whisker motion, touch and object localization,” said Dr. Oberlaender and he concluded, “This will take us one step closer to understanding how the brain transforms sensory information into behavioral responses”.

More information: Oberlaender, M., et al. (2011). Three-dimensional axon morphologies of individual layer 5 neurons indicate cell type-specific intracortical pathways for whisker motion and touch. Proc. Natl. Acad. Sci. USA

Provided by Max-Planck-Gesellschaft

Scientists discover anti-anxiety circuit in brain region considered the seat of fear

2011-03-10T05:46:00.000-08:00

A new study supports the role of a brain region called the amygdala in processing anxiety. In this 3-D magnetic resonance imaging (MRI) rendering of a human brain, functional MRI (fMRI) activation of the amygdala is highlighted in red. Credit: NIMH Clinical Brain Disorders Branch

Stimulation of a distinct brain circuit that lies within a brain structure typically associated with fearfulness produces the opposite effect: Its activity, instead of triggering or increasing anxiety, counters it.

That's the finding in a paper by Stanford University School of Medicine researchers to be published online March 9 in Nature. In the study, Karl Deisseroth, MD, PhD, and his colleagues employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals' willingness to take risks, while inhibiting its activity renders them more risk-averse. This discovery could lead to new treatments for anxiety disorders, said Deisseroth, an associate professor of bioengineering and of psychiatry and behavioral science.

The investigators were able to pinpoint this particular circuit only by working with a state-of-the-art technology called optogenetics, pioneered by Deisseroth at Stanford, which allows brain scientists to tease apart the complex circuits that compose the brain so these can be studied one by one.

"Anxiety is a poorly understood but common psychiatric disease," said Deisseroth, who is also a practicing psychiatrist. More than one in four people, in the course of their lives, experience bouts of anxiety symptoms sufficiently enduring and intense to be classified as a full-blown psychiatric disorder. In addition, anxiety is a significant contributing factor in other major psychiatric disorders from depression to alcohol dependence, Deisseroth said.

Most current anti-anxiety medications work by suppressing activity in the brain circuitry that generates anxiety or increases anxiety levels. Many of these drugs are not very effective, and those that are have significant side effects such as addiction or respiratory suppression, Deisseroth said. "The discovery of a novel circuit whose action is to reduce anxiety, rather than increase it, could point to an entire strategy of anti-anxiety treatment," he added.

Ironically, the anti-anxiety circuit is nestled within a brain structure, the amygdala, long known to be associated with fear. Generally, stimulating nervous activity in the amygdala is best known to heighten anxiety. So the anti-anxiety circuit probably would have been difficult if not impossible to locate had it not been for optogenetics, a new technology in which nerve cells in living animals are rendered photosensitive so that action in these cells can be turned on or off by different wavelengths of light. The technique allows researchers to selectively photosensitize particular sets of nerve cells. Moreover, by delivering pulses of light via optical fibers to specific brain areas, scientists can target not only particular nerve-cell types but also particular cell-to-cell connections or nervous pathways leading from one brain region to another. The fiber-optic hookup is both flexible and pain-free, so experimental animals' actual behavior as well as their brain activity can be monitored.

In contrast, older research approaches involve probing brain areas with electrodes to stimulate nerve cell firing. But an electrode stimulates not only all the nerve cells that happen to be in the neighborhood but even fibers that are just passing through on the way to somewhere else. Thus, any effect from stimulating the newly discovered anti-anxiety circuit would have been swamped by the anxiety-increasing effects of the dominant surrounding circuitry.

In December 2010, the journal Nature Methods bestowed its "Method of the Year" title on optogenetics.

In the new Nature study, the researchers photosensitized a set of fibers projecting from cells in one nervous "switchboard" to another one within the amygdala. By carefully positioning their light-delivery system, they were able to selectively target this projection, so that it alone was activated when light was pulsed into the mice's brains. Doing so led instantaneously to dramatic changes in the animals' behavior.

"The mice suddenly became much more comfortable in situations they would ordinarily perceive as dangerous and, therefore, be quite anxious in," said Deisseroth. For example, rodents ordinarily try to avoid wide-open spaces such as fields, because such places leave them exposed to predators. But in a standard setup simulating both open and covered areas, the mice's willingness to explore the open areas increased profoundly as soon as light was pulsed into the novel brain circuit. Pulsing that same circuit with a different, inhibitory frequency of light produced the opposite result: the mice instantly became more anxious. "They just hunkered down" in the relatively secluded areas of the test scenario, Deisseroth said.

Standard laboratory gauges of electrical activity in specific areas of the mice's amygdalas confirmed that the novel circuit's activation tracked the animals' increased risk-taking propensity.

Deisseroth said he believes his team's findings in mice will apply to humans as well. "We know that the amygdala is structured similarly in mice and humans," he said. And just over a year ago a Stanford team led by Deisseroth's associate, Amit Etkin, MD, PhD, assistant professor of psychiatry and behavioral science, used functional imaging techniques to show that human beings suffering from generalized anxiety disorder had altered connectivity in the same brain regions within the amygdala that Deisseroth's group has implicated optogenetically in mice.

Provided by Stanford University Medical Center

Can the brain explain your mind?

2011-03-07T06:50:00.000-08:00

Immune molecule regulates brain connections

2011-03-01T06:40:00.000-08:00

Immune molecule regulates brain connections
February 27th, 2011 in Medicine & Health / Neuroscience

The number of connections between nerve cells in the brain can be regulated by an immune system molecule, according to a new study from UC Davis. The research, published Feb. 27 in the journal Nature Neuroscience, reveals a potential link between immunity, infectious disease and conditions such as schizophrenia or autism.

Schizophrenia, autism and other disorders are associated with changes in connectivity in the brain, said Kimberley McAllister, associate professor in the Center for Neuroscience and Departments of Neurology and Neurobiology, Physiology and Behavior at UC Davis. Those changes affect the ability of the brain to process information correctly.

"Certain immune genes and immune dysregulation have also been associated with autism and schizophrenia, and the immune molecules that we study in brain development could be a pathway that contributes to that altered connectivity," McAllister said.

The study does not show a direct link between immune responses and autism, but rather reveals a molecular pathway through which a peripheral immune response or particular genetic profile could alter early brain development, McAllister said.

The researchers looked at a protein called Major Histocompatibility Complex type 1 (MHC type I). In both rodents and humans, these proteins vary between individuals, and allow the immune system to distinguish between 'self' and 'non-self.' They play a role, for example, in rejecting transplanted organs and in defending against cancer and virus infections.

In this and another recently published study, McAllister's group found that MHC type I molecules are present on young brain cells during early postnatal development. To test their function, they studied mice lacking MHC type I on the surface of neurons, as well as isolated neurons from mice and rats with altered levels of MHC type I. They found that when the density of these molecules on the surface of a brain cell goes up, the number of connections, or synapses, it has with neighboring brain cells goes down. The reverse was also true: decreased MHC expression increased synaptic connections.

"The effect on synapse density was mediated through MHC type I proteins," McAllister said.

"But these immune proteins don't just regulate synapse density, they also determine the balance of excitation and inhibition on young neurons -- a property critical for information processing and plasticity in young brains."

Expression of MHCI on neurons was itself regulated by neural activity, the team found, and MHCI mediated the ability of neural activity to alter synaptic connections.

About 10 years ago, other researchers discovered that MHC type I is involved in elimination of connections during a critical period of late postnatal brain development.

"We have now found that there is another role for MHC type I in establishing connections during early postnatal development of the brain," McAllister said.

Provided by University of California - Davis

"Les jeux vidéo et les réseaux sociaux modifient le rapport à l'espace, au temps, à la construction de l'identité"

2011-02-28T19:46:00.000-08:00

Ice Berg : Les "psy" constatent-ils une augmentation des consultations pour des problèmes relationnels ou de comportement liés à l'utilisation grandissante et précoce des écrans ?

Oui, les psychologues et les psychiatres sont aujourd'hui énormément consultés pour l'usage jugé excessif des jeux vidéo ou des nouveaux réseaux sociaux.

Pol : Comprenez-vous l'angoisse des parents sur ce sujet ou la trouvez-vous disproportionnée ?

Les parents ont raison d'être inquiets, mais pas pour la raison qu'ils croient. La consommation excessive d'écrans à l'adolescence n'est, en règle générale, pas le signe de troubles psychologiques. En revanche, c'est vrai que la fréquentation excessive des écrans peut nuire à d'autres activités, et les parents doivent la réguler.

Tom : Pendant quelle durée quotidienne doit-on autoriser les enfants à être devant des écrans (ordinateur, télévision) ?

L'Académie américaine de pédiatrie a proposé en 1999 un guide pour les parents : pas d'écran avant 2 ans (les spécialistes s'accordent aujourd'hui à parler de 3 ans), une heure par jour entre 3 et 6 ans, 2 heures entre 6-9 ans et 3 heures au-delà. Mais il s'agit de temps réel global, incluant la télévision, l'ordinateur pour jouer, l'ordinateur pour travailler, la console portable...

Yan : La télévision et les jeux vidéo font partie de leur époque et de leur quotidien. Comment ne pas les mettre en marge sans tout leur interdire et rentrer en conflit avec leur désir qui semble d'être en phase avec leur temps ?

Pourquoi dit-on que les parents doivent cadrer le temps de jeu ? Parce qu'à l'adolescence, les jeunes n'ont pas encore acquis la possibilité de réguler eux-mêmes leurs impulsions. Ils ont de la difficulté à suivre les décisions qu'ils jugent pourtant les plus raisonnables pour eux. C'est pourquoi les parents doivent veiller à ce que les jeux vidéo n'occupent qu'une partie du temps de loisirs. Mais en même temps, cadrer est totalement insuffisant. Parce que les jeux vidéo comportent beaucoup d'aspects positifs et que les parents ont tout à gagner à s'y intéresser.

Quand les parents accompagnent en s'intéressant aux jeux de leurs enfants, ils savent cadrer avec beaucoup plus d'intelligence et d'efficacité. Cadrer sans accompagner est aussi inutile que vouloir accompagner sans cadrer. Les deux sont indispensables.

Latemotiv : Un enfant face à tous ces écrans peut-il devenir fou ? Et perdre la relation au réel ?

Jlrenck : Qu'en est-il des repères d'espace et de temps chez des jeunes rivés sur ces fenêtres "magiques" par lesquelles – virtuellement – les distances s'abolissent, et l'immédiat devient la norme ? Des signes perceptibles de "mutations", d'incompétences spatio-temporelles, etc., ont-ils été observés ?

La pratique des jeux vidéo, comme celle des nouveaux réseaux sociaux, modifie le rapport à l'espace, au temps, à la construction de l'identité, et à la place que nous donnons aux activités partagées et aux activités solitaires.

Mais une semblable révolution a déjà accompagné d'autres grandes innovations comme l'invention de l'écriture, et, dans une moindre mesure, de la diffusion du livre grâce à l'imprimerie. Les modes de fonctionnement nouveaux repérés chez les enfants et les adolescents ne sont ni meilleurs ni pires que ceux auxquels nous sommes traditionnellement familiers.

La culture des écrans est en train de remplacer celle du livre. Face à ce bouleversement, le pourcentage d'enfants présentant des troubles mentaux reste stable, et eux seuls courent le risque de développer des pathologies. Il ne faut pas confondre la sphère d'activité dans laquelle une pathologie est repérée avec la cause de celle-ci.

Docteur Olive : L'écran est-il comparable à de la drogue, tant au niveau chimique (dopamine...) que psychologique ?

Elvire : L'utilisation quotidienne de consoles de jeux ou d'Internet ne peut-elle pas générer des mécanismes addictifs chez les enfants ? Je constate que mes enfants ont parfois du mal à "décrocher" si je ne les y invite pas fermement.

Dans les années 1990, Aviel Goodman a développé l'idée qu'il existerait des addictions sans substance. Mais à ce jour, il n'y a pas de consensus des spécialistes sur l'existence d'une addiction à l'Internet, au virtuel ou aux jeux vidéo. Pourquoi ? Parce que plus ces jeux évoluent, et plus ils donnent de l'importance à la socialisation via Internet.

Evidemment, l'être humain adore échanger, ou plus précisément bavarder, et nous connaissons tous cela. Mais on ne peut pas dire pour autant qu'il existe une addiction au bavardage. Et c'est ce que font aujourd'hui la plupart des adolescents quand ils vont sur les jeux vidéo ou les réseaux sociaux : bavarder avec leurs copains. Le seul problème est chez ceux qui vont dans les jeux vidéo pour jouer seuls. C'est pourquoi les parents doivent toujours poser la question à leur enfant : "est-ce que tu joues seul ou avec d'autres ?" Jouer seul est le plus inquiétant, et si l'enfant répond qu'il joue avec d'autres, il faut lui demander s'il joue avec d'autres qu'il connaît ou qu'il ne connaît pas. La réponse la plus rassurante est celle où il retrouve le soir dans ses jeux des camarades de classe qu'il côtoie la journée.

Adrien : Les réseaux sociaux ne sont-ils pas des lames à double tranchant : d'un côté, l'incroyable possibilité pour qui l'utilise d'échanger en temps réel et, de l'autre, un cloisonnement autour d'un écran, une certaine solitude face à l'écran ?

Dans les réseaux sociaux, on n'est jamais seul, par définition. D'autant plus que des études ont montré que les jeunes, à la différence des adultes, retrouvent préférentiellement dans ces réseaux des personnes de leur âge, qu'ils connaissent par ailleurs. Les adultes cherchent plutôt à rencontrer des inconnus, avec le désir d'avoir des aventures...

Lapin : L'écran ne risque-t-il pas de remplacer le parent en terme de transmission de normes et de valeurs ?

Il y a longtemps que les enfants cherchent dans les écrans des repères pour savoir comment devenir "grand". La télévision et le cinéma ont toujours constitué de tels repères. Et à partir de là, tout se joue autour de la relation que les enfants ont avec leurs parents. Si ceux-ci fonctionnent selon des règles claires et fiables, les enfants renoncent vite à appliquer les recettes qu'il leur semble découvrir sur les écrans. Mais si les parents n'ont pas de tels repères, ou, pire encore, se détournent de leurs enfants, ceux-ci vont évidemment tenter d'appliquer les modèles des écrans.

C'est la même chose aujourd'hui avec tout ce qu'ils trouvent sur Internet. S'il y a une différence, elle est seulement dans le fait que sur Internet, ils sont non seulement en contact avec des modèles, mais aussi avec la communauté de leurs camarades, ceux qu'on appelle les pairs. C'est pourquoi aujourd'hui, les enfants sont beaucoup plus dépendants des modèles pratiqués par leurs camarades que par le passé. Mais, comme par le passé, la capacité des parents de proposer des repères fiables et récurrents reste essentielle.

Mimie : Je n'ai pas la télé à la maison, seulement un ordinateur sur lequel mes enfants regardent de courts dessins animés. Je passe pour un extra-terrestre mais je me dis que c'est mieux comme ça. Mais cela peut aussi être à double tranchant...

De plus en plus de parents préoccupés par l'influence des écrans sur leurs enfants préfèrent leur mettre des DVD plutôt qu'allumer la télévision. Les règles fixées par l'Académie américaine de pédiatrie en 1999 doivent s'appliquer de la même manière pour ce qui concerne le temps d'écran.

Mais cette formule présente un avantage considérable : permettre à l'enfant de choisir ce qu'il va regarder, de le regarder plusieurs fois s'il en a envie, ce qui lui permet de comprendre mieux l'histoire et de développer sa mémoire. En revanche, ce choix peut conduire l'enfant à ignorer l'existence de feuilletons ou de dessins animés dont ses camarades vont lui parler. Mais l'expérience montre que les enfants dans cette situation s'en débrouillent très bien et qu'il n'y a pas d'inquiétude à avoir, d'autant plus qu'ils s'arrangent toujours pour regarder la télévision chez leurs copains ou... chez leurs grands-parents.

Si les parents n'allument jamais la télévision, il vaut mieux qu'ils expliquent à leur enfant que c'est leur choix mais qu'ils sont tout à fait disposés quand même à parler de ce que l'enfant pourra voir ailleurs qu'à la maison.

Glagla : Les adultes ne sont-ils pas les premiers à donner le "mauvais exemple" en passant eux-mêmes de nombreuses heures chaque semaine à consulter leurs mails ou à échanger avec leurs amis sur les réseaux sociaux ?

Une récente étude américaine a montré que les enfants qui regardent le plus la télévision sont ceux dont les parents regardent le plus la télévision... Autrement dit, si des parents veulent que leurs enfants la regardent moins, le mieux est qu'ils commencent eux-mêmes par réduire leur propre temps d'écran.

Pour ce qui concerne l'utilisation des jeux vidéo en réseau, il semblerait que le fait d'avoir un parent qui joue est plutôt dissuasif pour l'enfant de jouer : le jeu vidéo est en effet vécu comme une manière de fuir les parents, et si eux-mêmes sont joueurs, l'enfant court toujours le risque de se voir donner des conseils qui l'empêcheront de cultiver l'illusion de fuir l'influence des parents, notamment du père.

Enfin, pour ce qui concerne les nouveaux réseaux sociaux, les jeunes y créent leur propre territoire, quel que soit l'usage que les parents en font de leur côté. Finalement, à mon avis, l'important est plutôt de créer dans la famille des moments où chacun peut parler de ses propres usages des écrans. Et le moment privilégié pour cela me paraît être le repas du soir pris en commun... sans écran, justement pour parler des écrans.

Jos : Quels sont les réels désagréments d'une pratique excessive des écrans chez les jeunes enfants (3-6 ans) ? Pouvez-vous les décrire précisément ?

Entre 3 et 6 ans, des études ont montré qu'il est essentiel que l'enfant ait des activités impliquant l'utilisation de ses dix doigts. C'est pour cela que traditionnellement, l'enfant à cet âge était invité à réaliser des découpages, des pliages, des collages, des coloriages... C'est en effet cette activité des dix doigts qui permet la maturation des régions cérébrales qui permettent l'appréhension des objets en trois dimensions. C'est pourquoi il vaut mieux éviter le plus possible que l'enfant à cet âge-là utilise une console de jeu qui ne mobilise que deux ou quatre doigts. Et il faut en particulier bannir complètement les consoles mobiles (Nintendo DS ou PSP), qui accaparent toute l'attention de l'enfant.

Au-delà, le désagrément principal est la réduction des autres activités et la réduction du temps disponible pour en avoir. Il y a tellement de choses à apprendre à cet âge.

Mais on ne peut pas non plus mettre sur le même plan la pratique d'un jeu vidéo et l'exploration de sites Internet. Pour un temps d'écran égal, prendre en compte le type d'activité est essentiel. Tout ce qui socialise l'enfant à travers l'écran et tout ce qui l'invite à se poser des questions et à résoudre des problèmes imprévus, favorise son développement. A l'inverse, toutes les activités de jeu répétitives, stéréotypées, et plus encore solitaires, sont inquiétantes.

Destouche : Que pensez-vous des projets de l'éducation nationale qui veut que les NTICE (nouvelles technologies de l’information, de la communication, et de l’enseignement) envahissent le champ éducatif et que les écoles deviennent des cyber-cafés ?

Le corps enseignant n'est pas prêt à laisser transformer les écoles en cybercafés ! En revanche, l'école a un rôle capital à jouer (comme les parents, mais différemment d'eux) pour que les enfants soient introduits de la meilleure façon aux nouvelles technologies. L'école doit expliquer aux enfants dès l'école primaire les trois règles de base d'Internet : tout ce qu'on y met peut tomber dans le domaine public ; tout ce qu'on y met y restera éternellement ; et tout ce qu'on y trouve est sujet à caution, parce qu'il est impossible de repérer les images de la réalité des images falsifiées.

L'école a également un rôle essentiel à jouer pour expliquer aux enfants les modèles économiques qui sous-tendent Facebook, YouTube, Dailymotion..., et aussi l'importance du droit à la dignité et du droit à l'image. Avant d'être un lieu où l'on utilise les nouvelles technologies, l 'école doit être un lieu où les enseignants les connaissent suffisamment pour mettre les enfants en garde contre leurs dangers et leurs pièges.

Quant à l'utilisation des nouvelles technologies à l'école, les modèles sont encore à l'étude. On s'oriente aujourd'hui dans deux directions : d'abord, la mise au point de jeux vidéo à travers lesquels les enfants puissent acquérir des apprentissages utiles (jeux qu'on appelle "serious games") ; et ensuite, l'utilisation des outils numériques que les enfants possèdent, à commencer par leur téléphone mobile et leur iPod. La meilleure manière qu'ils n'utilisent pas ces machines pour s'échapper des cours est encore de les obliger à travailler avec ! Mais nous ne sommes qu'au début de ces recherches.

Anna : Je constate (mes collègues aussi) chez mes élèves de 9 ans de grosses difficultés de concentration et une nette tendance au zapping. Est-ce lié aux jeux vidéo et à la télévision ?

Le cerveau des nouvelles générations, et d'ailleurs de tous ceux qui sont gros consommateurs de nouvelles technologies, ne fonctionne plus comme par le passé. Le désir d'obtenir une réponse rapide, le fait de passer rapidement d'un sujet à un autre, la difficulté de concentration, tout cela fait partie des nouvelles façons de fonctionner. C'est vrai qu'elles sont inadaptées au système d'enseignement traditionnel. Mais le problème est que rien ne prouve à ce jour qu'elles soient inadaptées au fonctionnement qui sera exigé de chacun d'entre nous dans dix ou vingt ans. On voit déjà de jeunes employés qui sont incapables de se concentrer sur une seule tâche et passent sans cesse de l'une à l'autre pour les résoudre en parallèle, et non plus successivement. C'est très déroutant pour les vieux cadres qui les regardent. Mais ils arrivent à faire le travail pas plus mal que leurs aînés, même si la méthode paraît dérouter la logique qui veut qu'on résolve plusieurs tâches de natures différentes les unes après les autres. Voilà le genre de paradoxe auquel il faut nous habituer.

Certains pédagogues américains suggèrent même que la seule chose qu'il faudrait apprendre aux élèves serait la programmation de machines, car demain l'humanité se divisera en deux : ceux qui savent les utiliser (pensons à nos smartphones d'aujourd'hui !) et ceux qui sauront si mal le faire qu'ils seront rapidement marginalisés. C'est pourquoi les enseignants doivent s'engager eux-mêmes dans l'usage des nouvelles technologies pour mesurer l'ampleur des bouleversements qu'elles imposent au fonctionnement psychique et aux procédures d'apprentissage, et relativiser leurs dangers possibles.

Didon : Comment choisir les dessins animés que peuvent regarder des petits enfants à partir de 2 ans et demi ?

Rappelez-vous que le Conseil supérieur de l'audiovisuel a repris à son compte le slogan "Pas d'écran avant 3 ans". Cela ne signifie pas qu'un enfant soit menacé dans son développement s'il regarde une demi-heure ou une heure de télévision par jour. Mais cela signifie qu'il a toujours mieux à faire, parce qu'à cet âge-là, ce qui importe, c'est qu'il puisse interagir avec le monde environnant d'une manière qui fasse intervenir tous ses sens.

La télévision nous offre une relation réduite à la vue et à l'audition. Si un enfant n'a jamais l'occasion de regarder les programmes que les parents regardent pour eux, pourquoi en effet ne pas lui mettre de temps en temps un dessin animé ? Mais avant l'âge de 3 ans, et même un peu au-delà, il n'y comprendra rien de toute façon. Seuls comptent le rythme, qui doit plutôt être lent, et les couleurs, plutôt harmonieuses...

Tom : Pensez-vous qu'il y a un âge limite pour avoir un téléphone portable ?

L'âge auquel les parents achètent un téléphone portable à leur enfant baisse de plus en plus. Il n'est pas rare aujourd'hui de voir des enfants en posséder en CM1. La seule chose que je peux dire aux parents, c'est que plus tôt un enfant aura un téléphone portable, et plus rapidement il s'éloignera de ses parents. A partir de là, tout dépend donc de leurchoix...

The Regimen of Bodily Health: Nourishment and Natural Knowledge

2011-02-26T13:58:00.000-08:00

Cursos de Neuroartes en Tijuana. Marzo 2011.

2011-02-25T15:07:00.000-08:00

Meditation beats dance for harmonizing body and mind

2011-02-25T05:27:00.000-08:00

Meditation beats dance for harmonizing body and mind
February 24th, 2011 in Medicine & Health / Psychology & Psychiatry
Enlarge

The body is a dancer's instrument, but is it attuned to the mind? A new study from the University of California, Berkeley, suggests that professional ballet and modern dancers are not as emotionally in sync with their bodies as are people who regularly practice meditation.

UC Berkeley researchers tracked how closely the emotions of seasoned meditators and professional dancers followed bodily changes such as breathing and heart rates.

They found that dancers who devote enormous time and effort to developing awareness of and precise control over their muscles – a theme coincidentally raised in the new ballet movie “Black Swan” – do not have a stronger mind-body connection than do most other people.

By contrast, veteran practitioners of Vipassana or mindfulness meditation – a technique focused on observing breathing, heartbeat, thoughts and feelings without judgment – showed the closest mind-body bond, according to the study recently published in the journal Emotion.

“We all talk about our emotions as if they are intimately connected to our bodies – such as the ‘heartache of sadness’ and ‘bursting a blood vessel’ in anger,” said Robert Levenson, a UC Berkeley psychology professor and senior author of the study. “We sought to precisely measure how close that connection was, and found it was stronger for meditators.”

The results offer new clues in the mystery of the mind-body connection. Previous studies have linked the dissociation of mind and body to various medical and psychiatric diseases.

“Ever have the experience of getting home from work and realizing you have a blistering headache?” said Jocelyn Sze, a doctoral student in clinical science at UC Berkeley and the lead author of the study. “The headache probably built up throughout the day, but you might have been intentionally ignoring it and convincing yourself that you felt fine so that you could get through the demands of the day.”

Increasingly, mindfulness meditation is being used to treat physical and psychological problems, researchers point out. “We believe that some of these health benefits derive from meditation’s capacity to increase the association between mind and body in emotion,” Levenson said.

For the experiment, the researchers recruited volunteers from meditation and dance centers around the San Francisco Bay Area and via Craigslist. The study sample consisted of 21 dancers with at least two years of training in modern dance or ballet and 21 seasoned meditators with at least two years of Vipassana practice. A third “control group” was made up of 21 moderately active adults with no training in dance, meditation, Pilates or professional sports.

Participants, who ranged in age from 18 to 40, were wired with electrodes to measure their bodily responses while they watched emotionally charged scenes from movies and used a rating dial to indicate how they were feeling.

Although all participants reported similar emotional reactions to the film clips, meditators showed stronger correlations between the emotions they reported feeling and the speed of their heartbeats. Surprisingly, the differences between dancers and the control group were minimal.

Researchers theorize that dancers learn to shift focus between time, music, space, and muscles and achieve heightened awareness of their muscle tone, body alignment and posture.

“These are all very helpful for becoming a better dancer, but they do not tighten the links between mind and body in emotion,” Levenson said.

By contrast, meditators practice attending to “visceral” body sensations, which makes them more attuned to internal organs such as the heart. “These types of visceral sensations are a primary focus of Vipassana meditation, which is typically done sitting still and paying attention to internal sensations,” Sze said.

More information: The study was published in the December 2010 issue of Emotion.

Provided by University of California - Berkeley

Brain's 'reward' center also responds to bad experiences

2011-02-24T05:16:00.000-08:00

Brain's 'reward' center also responds to bad experiences
February 22nd, 2011 in Medicine & Health / Neuroscience

Dr. Joe Z. Tsien of Georgia Health Sciences University has shown that the "reward" center of the brain also responds to bad experiences. Credit: Phil Jones/GHSU Photographer

The so-called reward center of the brain may need a new name, say scientists who have shown it responds to good and bad experiences. The finding, published in PLoS One, may help explain the "thrill" of thrill-seeking behavior or maybe just the thrill of surviving it, according to scientists at Georgia Health Sciences University and East China Normal University.

Eating chocolate or falling off a building – or just the thought of either – can evoke production of dopamine, a neurotransmitter that can make the heart race and motivate behavior, said Dr. Joe Z. Tsien, Co-Director of GHSU's Brain & Behavior Discovery Institute.

Scientists looked at dopamine neurons in the ventral tegmental area of the mouse brain, widely studied for its role in reward-related motivation or drug addiction. They found essentially all the cells had some response to good or bad experiences while a fearful event excited about 25 percent of the neurons, spurring more dopamine production.

Interestingly neuronal response lasted as long as the event and context was important, Tsien said. Scientists used a conditioned tone to correlate a certain setting with a good or bad event and later, all it took was the tone in that setting to evoke the same response from the dopamine neurons of mice.

"We have believed that dopamine was always engaged in reward and processing the hedonic feeling," Tsien said. "What we have found is that dopamine neurons also are stimulated or respond to negative events."

Just how eating chocolate or jumping off a building induces dopamine production remains a mystery. "That is just the way the brain is wired," Tsien said. He notes that genetics can impact the number of cells activated by bad events – and while interpretation of the findings needs more work – they could help explain inappropriate behaviors such as drug addiction or other risky habits.

In a second paper in PLoS One, Tsien and his colleagues at Boston University have provided more insight into how brains decide how much to remember good or bad. Inside the hippocampus, where memory and knowledge are believe to be formed, recordings from hundreds of mouse brain cells in a region called CA1 showed all are involved in sensing what happens, but not in the same way.

They found among most cells a big event, such as a major earthquake, evoked a bigger sensory response than a mild earthquake. But slightly less than half the cells involved logged a more consistent neural response to all events big and small. These are called invariant cells because of their consistent firing regardless of event intensity. Tsien said these cells are critical in helping the brain remember those events.

The initial muted sensory response was followed by the cells replaying what they just experienced. It's that reverberation that corresponds with learning and memory. "If they play it over and over, you can remember it for a long time," Tsien said of these memory makers.

But these invariant cells vary in that some keep replaying specific memories while the majority focus on more general features of what occurred. "The general-knowledge cells have the 'highest volume,'" Tsien said. "So we walk away with general knowledge that will guide your life, which is more important than the details."

As with the number of dopamine cells that respond to bad or risky behavior, genetics likely plays a role in an individual's specific ratio of cells involved in encoding general versus more detailed memories, Tsien said. A person with a photographic memory likely has more of the specific memory makers while those with autism or schizophrenia, who have difficulty coping in society, may have fewer of the general memory makers that help provide correct context and understanding of complex relationships.

Provided by Georgia Health Sciences University

Look after your brain

2011-02-22T05:42:00.001-08:00

Look after your brain
February 20th, 2011 in Medicine & Health / Diseases

As the average life span becomes longer, dementia becomes more common. Swedish scientist Laura Fratiglioni has shown that everyone can minimize his or her risk of being affected. Factors from blood pressure and weight to the degree of physical and mental activity can influence cognitive functioning as one gets older.

The lengthening of the average life span in the population has caused an increase in the prevalence of aging related disorders, one of which is cognitive impairment and dementia. An expert panel estimates that worldwide more than 24 million people are affected by dementia, most suffering from Alzheimer's disease. In the more developed countries, 70 percent of the persons with dementia are 75 years or older.

Age is the greatest risk factor for developing dementia. But there is growing evidence that the strong association with increasing age can be, at least partially, explained by a life course cumulative exposure to different risk factors.

Laura Fratiglioni's research group at Karolinska Institutet is a leader in identifying the risk factors that lie behind developing dementia and using this knowledge to develop possible preventative strategies. The group's research has shown that the risk is partly determined by an individual genetic susceptibility, and that active involvement in mental, physical and social activities can delay the onset of dementia by preserving cognitive functions. Further education early in life has a protective effect, and the group's research has shown that it is never too late to get started.

"The brain, just as other parts of the body, requires stimulation and exercise in order to continue to function. Elderly people with an active life – mentally, physically and socially – run a lower risk of developing dementia, and it doesn't matter what the particular activities are", says Professor Laura Fratiglioni.

Laura Fratiglioni's research has shown that physical factors are also significant. Not only high and low blood pressure, but also diabetes and obesity when middle-aged increase the risk of developing dementia after the age of 70. "What is good for the heart is good for the brain", she says.

Knowledge about risk factors and how to protect the brain from dementia is based on observational studies in which scientists have discovered statistical correlations in the population. Scientists in other current studies that are carried out in Europe are investigating what happens when a large number of study participants are given special help to better control vascular risk factors and to stimulate social, physical and mental activities. which should, at least, lead to a delay of dementia onset.

"You could say that we are progressing from observation to experiment. This means that in a few years we will know more about which strategies are most effective in preventing neurodegenerative disorders", says Laura Fratiglioni.

Provided by Karolinska Institutet

Model-driven therapeutic treatment of neurological disorders: reshaping brain rhythms with neuromodulation

2011-02-19T06:50:00.001-08:00

Model-driven therapeutic treatment of neurological disorders: reshaping brain rhythms with neuromodulation
Julien Modolo 1,2, Alexandre Legros 1,2, Alex W. Thomas 1,2 and Anne Beuter 1,3

1Lawson Health Research Institute, St Joseph Health Care, 268 Grosvenor Street, London, Canada
2Department of Medical Biophysics, University of Western Ontario, London, Canada
3Bordeaux Polytechnic Institute, University of Bordeaux, 16 avenue Pey-Berland, Pessac, France
*Author for correspondence (anne.beuter@ensc.fr).
Abstract
Electric stimulation has been investigated for several decades to treat, with various degrees of success, a broad spectrum of neurological disorders. Historically, the development of these methods has been largely empirical but has led to a remarkably efficient, yet invasive treatment: deep brain stimulation (DBS). However, the efficiency of DBS is limited by our lack of understanding of the underlying physiological mechanisms and by the complex relationship existing between brain processing and behaviour. Biophysical modelling of brain activity, describing multi-scale spatio-temporal patterns of neuronal activity using a mathematical model and taking into account the physical properties of brain tissue, represents one way to fill this gap. In this review, we illustrate how biophysical modelling is beginning to emerge as a driving force orienting the development of innovative brain stimulation methods that may move DBS forward. We present examples of modelling works that have provided fruitful insights in regards to DBS underlying mechanisms, and others that also suggest potential improvements for this neurosurgical procedure. The reviewed literature emphasizes that biophysical modelling is a valuable tool to assist a rational development of electrical and/or magnetic brain stimulation methods tailored to both the disease and the patient's characteristics.

Source: The Royal Society
http://rsfs.royalsocietypublishing.org/content/1/1/61.abstract?etoc

Biologists gain new insights into brain circuit wiring

2011-02-16T06:28:00.000-08:00

Biologists gain new insights into brain circuit wiring
February 14th, 2011 in Medicine & Health / Neuroscience

Neurobiologists at UC San Diego have discovered new ways by which nerves are guided to grow in highly directed ways to wire the brain during embryonic development.

Their finding, detailed in a paper in the February 15 issue of the journal Developmental Cell, provides a critical piece of understanding to the longstanding puzzle of how the human brain wires itself into the complex networks that underlie our behavior.

The discovery concerns the movements of a highly sensitive and motile structure at the tips of growing nerves called a growth cone. For more than a century, biologists have known that growth cones find their targets by detecting chemical cues in the developing nervous system. They do that by responding to gradients of chemical concentration and steering nerve cells either up or down the gradient to eventually find the right targets to make the proper nerve connections that then establish neuronal networks.

While many of these chemical guidance cues have been identified over the past decade, scientists still don't fully understand how the growth cone picks up small concentration differences in the developing embryo or how guidance cues enter the growth cone to regulate the cellular machinery to turn growth cones in one direction or another.

Yimin Zou, an associate professor of neurobiology at UC San Diego, and his colleagues had previously shown that a family of proteins known as "Wnt morphogens" provide the directional cues for the wiring of circuits in many parts of the developing brain.

"These morphogens are often strategically placed in important organizing centers of the developing nervous system and play a major role in sculpting brain connections," said Zou.

In their latest paper, Zou and his UCSD colleagues, Beth Shafer, Keisuke Onishi, Charles Lo and Gulsen Colakoglu, report their discovery that Wnt proteins steer the growth cone by stimulating planar cell polarity signaling.

"Planar cell polarity or PCP refers to the polarized structures and functions of a sheet of epithelial cells along the plane of the tissue," he said. "The direction of our skin hair in our backs, for example, is polarized to point down from our head and a highly conserved genetic program, the PCP signaling system, ensures this type of tissue organization in our skin as well as many other parts of our body."

The UCSD research team found that the growth cone is equipped with all the PCP components necessary to steer extensions of nerve cells, or axons, to their proper targets within the Wnt gradients.

"This study reveals a novel type of environmental signal which the growth cone responds to, previously unknown to developmental neurobiologists, the tissue polarity signals," said Zou. "Tissue polarity is a long lasting structural feature and may provide organizational information to axonal connections while the brain is being wired up. Because PCP signaling is essential for the beautifully organized structures in the brain, the brain may owe a large part of its stunning axonal organization to the function of PCP signaling. PCP signaling relies heavily on cell-cell interactions, which may pave way for developmental neuroscientists to understand how groups of neurons organize their axons into exquisite patterns."

The UCSD researchers also found that one of the PCP components, Vangl2, is highly enriched on the tips of growing filopodia on the growth cone.

"The filopodia are the motile structures that explore the environment," said Zou. "It has been long speculated that the long filopodia can extend the span of the growth cone to sample larger concentration drops. The localization of Vangl2 on growth cone tips suggests that the tips are more sensitive to guidance cues than the rest of the growth cone."

"This paper not only reveals the profound logic of brain wiring mechanisms but also provides satisfactory and in-depth mechanistic insights," he added. "With these new insights and tools at hand, one can now move on to design experiments to ask the next level questions, such as the cell biological mechanisms of growth cone steering. These findings will also provide new methods for nervous system repair and regeneration."

Provided by University of California - San Diego

Communication breakdown: Early defects in sensory synapses in motor neuron disease

2011-02-10T05:37:00.000-08:00

Communication breakdown: Early defects in sensory synapses in motor neuron disease,
February 9th, 2011 in Medicine & Health / Neuroscience

New research using a mouse model of the motor neuron disease spinal muscular atrophy (SMA) reveals an abnormality in the way that sensory information is relayed to motor neurons in the spinal cord. Importantly, this disruption in communication occurs very early in disease progression and precedes the neuronal death and muscle weakness that are the hallmark of the disease. The study, published by Cell Press in the February 10 issue of the journal Neuron, suggests that therapeutic strategies designed to improve communication at these spinal synapses might help to slow or prevent the progression of the disease and should be further explored.

Amyotrophic lateral sclerosis (ALS) and SMA are human motor neuron diseases characterized by degeneration and death of motor neurons and the muscles that they innervate. Most research on motor neuron diseases has focused on the communication, or synapse, between the neuron and the muscle. However, because these motor neurons originate in the spinal cord and rely on inputs from sensory neurons as well as other neurons from different regions of the brain and spinal cord, it is possible that upstream events might contribute to disease pathology. "There is some evidence that spinal circuit abnormalities might occur in human motor neuron disease," explains the principal author of the study, Dr. George Z. Mentis, who moved last year to the Motor Neuron Center at Columbia University from the National Institute of Neurological Disease and Stroke, where the study was initiated. "However, little is known about the response of these synapses to the factors that trigger disease."

Using a mouse model of SMA that exhibits many of the features of human SMA, including a stereotypical pattern of progressive muscle weakness, Dr. Mentis and colleagues studied synaptic connections between sensory and motor neurons in the spinal cord. "We found that communication between the sensory and motor neurons that make up the stretch reflex, which is known to be important for motor function, showed massive and progressive failure early in the disease process," says Dr. Mentis. The functional deficit mirrored the pattern of muscle weakness in human SMA patients. The researchers went on to show that a drug that has been shown to improve motor function and increase survival of SMA mice improved the sensory-motor circuitry.

"Collectively, our findings suggest that spinal circuit dysfunction is one of the earliest and most pronounced pathological features of the disease and therefore may contribute significantly to the loss of motor function that characterize both mouse models and human SMA patients," concludes Dr. Mentis. "Our data also support the potential therapeutic use of drugs to improve synaptic function, which is likely to be a key factor in the restoration of normal motor function in this disease."

Provided by Cell Press

Researchers working on tiny, implantable computers to restore lost brain functions

2011-02-09T07:53:00.000-08:00

Researchers working on tiny, implantable computers to restore lost brain functions
February 8th, 2011 in Medicine & Health / Research

Dr. Eberhard Fetz at the University of Washington in Seattle is principal investigator on a W.M. Keck Foundation grant to develop tiny, implantable computers to restore brain functions lost to injury or disease. Credit: Leila Gray

Tiny, implantable computers that would restore brain function lost to disease or injury is the goal of University of Washington research recently funded by a $1 million, three-year grant from the W.M. Keck Foundation.

The UW has made significant progress in neural engineering – the study of communication and control between biological and machine systems. The Keck project is the next step in advancing the technology of miniature devices developed at the UW to record from and stimulate the brain, spinal cord and muscles.

The principal investigator on the Keck Foundation grant is Dr. Eberhard E. Fetz, UW professor of physiology and biophysics and a core staff researcher at the Washington National Primate Research Center. He and his colleagues have successfully deployed tiny, battery-powered implantable brain-computer interfaces called neurochips in animals.

The neurochip can record nerve cell activity in one part of the brain, process this activity and then stimulate cells in another brain region. The battery-powered device operates continuously during free behavior. When primates carry out their usual daily activities – socializing, climbing, eating, and exploring – their brains can learn to exploit these new resources under normal behavioral conditions.

One potential clinical application is to bridge lost biological connections. For example, the researchers have shown that monkeys can learn to bypass an anesthetic block in the nerves of the arm and to activate temporarily paralyzed muscles with activity of cortical neurons. In some ways the device acts as a volition processor, tapping into signals representing the will to move and using them to stimulate the paralyzed muscles to reach targets.

"Using an implantable computer interface to implement novel interactions between brain sites opens many fundamentally new research directions," Fetz said, "depending on the site of recording and stimulation, and how these signals are processed and transformed."

He explained that a second application is to promote neural plasticity, which could strengthen connections and allow some of the brain's functions to be rescued when impaired. This happens naturally when people recover the ability to move or speak again after a stroke or brain injury. The bidirectional brain computer interface could facilitate this recovery and exploit the brain's innate talent for re-organizing itself as it heals.

"We expect that the recurrent type of brain computer interface we are trying to develop," he added, "will eventually have numerous clinical applications for bridging damaged biological pathways and strengthening weak neural connections." For example, signals from the motor-control regions of the brain can be used to stimulate parts of the spinal cord to evoke coordinated movements. This would create connections that could replace lost pathways between the brain and spinal cord, a loss that occurs with strokes and spinal cord injuries.

Many labs around the world are working on brain-computer interfaces that convert neural activity to control of external devices such as prosthetic limbs or computer cursors. What makes the recently funded project unusual is that its scientists are developing a recurrent implantable device that would interact bidirectionally with the brain. By operating autonomously and continuously, without the need for connection to external instrumentation, it would facilitate long-term behavioral adaptation and plasticity.

The proposed research plans to develop this new paradigm to promote restoration of brain, spine, and muscle function. The work could eventually lead to miniaturized electrical and biological interfaces that operate around the clock on a small amount of power while the wearer goes about his or her usual activities, according to Fetz. He added that, if successful, this implantable technology would advance the ability of subjects to effectively control a brain computer interface by allowing long-term adaptation to consistent contingencies, and would open opportunities for the brain to exploit bidirectional interactions with miniature computers. This implementation of continuous reciprocal interaction goes beyond the existing paradigm of using brain signals to control external devices through tethered connections.

As part of the project the team also plans to create a powerful multichannel "Keck Active Electrode Array" with integrated electronics to record and stimulate large numbers of brain sites. This array would operate with electrodes on the surface of the brain and be less invasive than penetrating intracortical electrodes.

To overcome the many technical problems in creating safe, effective devices of this nature and realizing their clinical potential, the project depends on a team of UW experts in different fields.

Dr. Brian Otis, UW assistant professor of electrical engineering, has extensive experience in wireless sensors and in designing extremely small radios that can be incorporated into other devices. He is also an expert in bioelectronics and the processing of signals with minimal power. His group will design and miniaturize the low power circuitry for the computer and the signal amplifiers, and will work toward harvesting energy to operate the device, perhaps from the body's own heat or muscle activity.

Dr. Babak Parviz, the UW McMorrow Innovation Associate Professor of Electrical Engineering, has skill in the fabrication of micro- and nano-scale tools, self-assembled biocompatible machinery, and sensors for detecting very faint signals. His group will create the specialized electrode arrays for recording and stimulation, and will help integrate the miniature electronic systems used in the project.

Dr. Jeffrey Ojemann, UW professor of neurological surgery, has expanded his father's original studies on mapping of the human brain to identify critical areas for movement, language, memory and other functions prior to epilepsy surgery. He will bring his extensive knowledge of functional brain mapping and clinical recording of signals from the human brain to the project. He will help design and test the custom computer-enabled electrode arrays for potential applications to patient care.

Among the engineering and health issues the team will be addressing are integrating the electronics with the electrode array and making it small enough, finding a reliable source of the low power necessary to operate the system, evaluating any hazards the device might pose or serious long-term side effects, and developing biomaterials that won't cause irritation or be rejected, as well as meeting other safety, performance, and acceptability criteria.

"We are extremely grateful to the Keck Foundation for supporting this highly ambitious endeavor," Fetz said. "Looking ahead, we can anticipate that future innovations in nanotechnology, computers and brain science will advance this effort beyond the current state of the art. The grant allows us to be poised to incorporate these advances into the development of more powerful recurrent brain computer interfaces. We expect that these devices will have numerous applications in basic neuroscience research and as well as in clinical care."

Provided by University of Washington

Diplomado de Neuroartes en Tijuana.

2011-02-06T13:29:00.000-08:00

Why do we sleep?

2011-02-04T09:28:00.000-08:00

Why do we sleep?
February 3rd, 2011 in Medicine & Health / Research

Credit: Chau Dang, LTD Space

While we can more or less abstain from some basic biological urges—for food, drink, and sex—we can’t do the same for sleep. At some point, no matter how much espresso we drink, we just crash. And every animal that’s been studied, from the fruit fly to the frog, also exhibits some sort of sleep-like behavior. (Paul Sternberg, Morgan Professor of Biology, was one of the first to show that even a millimeter-long worm called a nematode falls into some sort of somnolent state.) But why do we—and the rest of the animal kingdom—sleep in the first place?

“We spend so much of our time sleeping that it must be doing something important,” says David Prober, assistant professor of biology and an expert on how genes and neurons regulate sleep. Yes, we snooze in order to rest and recuperate, but what that means at the molecular, genetic, or even cellular level remains a mystery. “Saying that we sleep because we’re tired is like saying we eat because we’re hungry,” Prober says. “That doesn’t explain why it’s better to eat some foods rather than others and what those different kinds of foods do for us.”

No one knows exactly why we slumber, Prober says, but there are four main hypotheses. The first is that sleeping allows the body to repair cells damaged by metabolic byproducts called free radicals. The production of these highly reactive substances increases during the day, when metabolism is faster. Indeed, scientists have found that the expression of genes involved in fixing cells gets kicked up a notch during sleep. This hypothesis is consistent with the fact that smaller animals, which tend to have higher metabolic rates (and therefore produce more free radicals), tend to sleep more. For example, some mice sleep for 20 hours a day, while giraffes and elephants only need two- to three-hour power naps.

Another idea is that sleep helps replenish fuel, which is burned while awake. One possible fuel is ATP, the all-purpose energy-carrying molecule, which creates an end product called adenosine when burned. So when ATP is low, adenosine is high, which tells the body that it’s time to sleep. While a postdoc at Harvard, Prober helped lead some experiments in which zebrafish were given drugs that prevented adenosine from latching onto receptor molecules, causing the fish to sleep less. But when given drugs with the opposite effect, they slept more. He has since expanded on these studies at Caltech.

Sleep might also be a time for your brain to do a little housekeeping. As you learn and absorb information throughout the day, you’re constantly generating new synapses, the junctions between neurons through which brain signals travel. But your skull has limited space, so bedtime might be when superfluous synapses are cleaned out.

And finally, during your daily slumber, your brain might be replaying the events of the day, reinforcing memory and learning. Thanos Siapas, associate professor of computation and neural systems, is one of several scientists who have done experiments that suggest this explanation for sleep. He and his colleagues looked at the brain activity of rats while the rodents ran through a maze and then again while they slept. The patterns were similar, suggesting the rats were reliving their day while asleep.

Of course, the real reason for sleep could be any combination of these four ideas, Prober says. Or perhaps only one of these hypotheses might have been true in the evolutionary past, but as organisms evolved, they developed additional uses for sleep.

Researchers in Prober’s lab look for the genetic and neural systems that affect zebrafish sleeping patterns by tweaking their genes and watching them doze off. An overhead camera records hundreds of tiny zebrafish larvae as they swim in an array of shallow square dishes. A computer automatically determines whether the fish are awake or not based on whether they’re moving or still, and whether they respond to various stimuli. Prober has identified about 500 drugs that affect their sleeping patterns, and now his lab is searching for the relevant genetic pathways. By studying the fish, the researchers hope to better understand sleep in more complex organisms like humans. “Even if we find only a few new genes, that’ll really open up the field,” he says. The future is promising, he adds, and for that, it’ll be well worth staying awake.

Provided by California Institute of Technology

Sleep selectively stores useful memories

2011-02-02T05:16:00.001-08:00

Sleep selectively stores useful memories
February 1st, 2011 in Medicine & Health / Neuroscience

After a good night's sleep, people remember information better when they know it will be useful in the future, according to a new study in the Feb. 2 issue of The Journal of Neuroscience. The findings suggest that the brain evaluates memories during sleep and preferentially retains the ones that are most relevant.

Humans take in large amounts of information every day. Most is encoded into memories by the brain and initially stored, but the majority of information is quickly forgotten. In this study, a team of researchers led by Jan Born, PhD, of the University of Lubeck in Germany set out to determine how the brain decides what to keep and what to forget.

"Our results show that memory consolidation during sleep indeed involves a basic selection process that determines which of the many pieces of the day's information is sent to long-term storage," Born said. "Our findings also indicate that information relevant for future demands is selected foremost for storage."

The researchers set up two experiments to test memory retrieval in a total of 191 volunteers. In the first experiment, people were asked to learn 40 pairs of words. Participants in the second experiment played a card game where they matched pictures of animals and objects — similar to the game Concentration — and also practiced sequences of finger taps.

In both groups, half the volunteers were told immediately following the tasks that they would be tested in 10 hours. In fact, all participants were later tested on how well they recalled their tasks.

Some, but not all, of the volunteers were allowed to sleep between the time they learned the tasks and the tests. As the authors expected, the people who slept performed better than those who didn't. But more importantly, only the people who slept and knew a test was coming had substantially improved memory recall.

The researchers also recorded electroencephalograms (EEG) from the individuals who were allowed to sleep. They found an increase in brain activity during deep or "slow wave" sleep when the volunteers knew they would be tested for memory recall.

"The more slow wave activity the sleeping participants had, the better their memory was during the recall test 10 hours later," Born said. Scientists have long thought that sleep is important in memory consolidation. The authors suggest that the brain's prefrontal cortex "tags" memories deemed relevant while awake and the hippocampus consolidates these memories during sleep.

Gilles Einstein, PhD, an expert in memory at Furman University, said the new findings help explain why you are more likely to remember a conversation about impending road construction than chitchat about yesterday's weather. "These results suggest that sleep is critical to this memory enhancement," said Einstein, who was unaffiliated with the study. "This benefit extends to both declarative memories (memory for a road detour) and procedural memories (memory for a new dance step)."

Provided by Society for Neuroscience

Neuroscientists find memory storage, reactivation process more complex than previously thought

2011-02-01T05:43:00.001-08:00

Neuroscientists find memory storage, reactivation process more complex than previously thought
January 31st, 2011 in Medicine & Health / Neuroscience

The process we use to store memories is more complex than previously thought, New York University neuroscientists have found. Their research, which appears in the journal the Proceedings of the National Academy of Sciences, underscores the challenges in addressing memory-related ailments, such as post-traumatic stress disorder.

The researchers looked at memory consolidation and reconsolidation. Memory consolidation is the neurological process we undergo to store memories after an experience. However, memory is dynamic and changes when new experiences bring to mind old memories. As a result, the act of remembering makes the memory vulnerable until it is stored again—this process is called reconsolidation. During this period, new information may be incorporated into the old memory.

It has been well-established that the synthesis of new proteins within neurons is necessary for memory storage. More specifically, this process is important for stabilizing memories because it triggers the production of new proteins that are required for molecular and synaptic changes during both consolidation and reconsolidation.

The purpose of the NYU study was to determine if there were differences between memory consolidation and reconsolidation during protein synthesis. Similar comparative studies have been conducted, but those focused on elongation, one of the latter stages of protein synthesis; the PNAS research considered the initiation stage, or the first step of this process.

Using laboratory rats as subjects, the researchers used mild electric shocks paired with an audible tone to generate a specific associative fear memory and, with it, memory consolidation. They played the audible tone one day later—a step designed to initiate recall of the earlier fear memory and bring about reconsolidation. During both of these steps, the rats were injected with a drug designed to inhibit the initiation stage of protein synthesis.

Their results showed that the inhibitor could effectively interfere with memory consolidation, but had no impact on memory reconsolidation.

"Our results show the different effects of specifically inhibiting the initiation of protein synthesis on memory consolidation and reconsolidation, making clear these two processes have greater variation than previously thought," explained Eric Klann, a professor at NYU's Center for Neural Science and one of the study's co-authors. "Because addressing memory-related afflictions, such at PTSD, depends on first understanding the nature of memory formation and the playback of those memories, finding remedies may prove even more challenging than is currently recognized."

Provided by New York University

Field of Attention for Instantaneous Object Recognition

2011-01-29T20:05:00.000-08:00

Field of Attention for Instantaneous Object Recognition

Jian-Gao Yao 1, Xin Gao 1, Hong-Mei Yan 1, Chao-Yi Li 1,2

1 Key Laboratory for Neuroinformatics, Ministry of Education of China, University of Electronic Sciences and Technology, Chengdu, China,
2 Center for Life Sciences, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai, China

Abstract
Background
Instantaneous object discrimination and categorization are fundamental cognitive capacities performed with the guidance of visual attention. Visual attention enables selection of a salient object within a limited area of the visual field; we referred to as “field of attention” (FA). Though there is some evidence concerning the spatial extent of object recognition, the following questions still remain unknown: (a) how large is the FA for rapid object categorization, (b) how accuracy of attention is distributed over the FA, and (c) how fast complex objects can be categorized when presented against backgrounds formed by natural scenes.

Methodology/Principal Findings
To answer these questions, we used a visual perceptual task in which subjects were asked to focus their attention on a point while being required to categorize briefly flashed (20 ms) photographs of natural scenes by indicating whether or not these contained an animal. By measuring the accuracy of categorization at different eccentricities from the fixation point, we were able to determine the spatial extent and the distribution of accuracy over the FA, as well as the speed of categorizing objects using stimulus onset asynchrony (SOA). Our results revealed that subjects are able to rapidly categorize complex natural images within about 0.1 s without eye movement, and showed that the FA for instantaneous image categorization covers a visual field extending 20°×24°, and accuracy was highest (>90%) at the center of FA and declined with increasing eccentricity.

Conclusions/Significance
In conclusion, human beings are able to categorize complex natural images at a glance over a large extent of the visual field without eye movement.

Beyond the bullet: Surviving a shot to the head carries host of challenges

2011-01-28T20:34:00.001-08:00

Beyond the bullet: Surviving a shot to the head carries host of challenges
January 28th, 2011 in Medicine & Health / Other

The spectral images, reproduced in neurosurgery journals and textbooks, could be captioned "Beauty and the Beast." Captured by X-ray and CT scan, the human brain is pierced by a bullet, nail, pool cue or chunk of razor-sharp debris. The intruding object has ripped a jagged vortex of destruction through the brain's gelatinous lobes and forged an even wider path of quivering shock.

If the projectile came in hard and fast, shards of broken skull will be scattered through the delicate tissue. The bullet might have ricocheted off bone and tumbled wildly in the cavity, bursting blood vessels and carving uneven holes where, only moments before, healthy brain cells had hummed.

Such havoc, you would think, would put an abrupt end to the brain's rhythmic buzz of activity and extinguish the life defined by its complex inner workings.

But - as the awakening of Rep. Gabrielle Giffords has demonstrated these last weeks - the human brain can be resilient, capable of withstanding brutish damage and then masterminding its reconstruction.

"I have seen every foreign body in the world pass through the brain, and I never cease to be amazed that some seem to survive and do amazingly well," said Dr. Ian Armstrong, a Century City, Calif., neurosurgeon, shortly after Giffords was shot.

Make no mistake: Bullets usually kill when they enter the brain. The U.S. Centers for Disease Control and Prevention estimates that in 90 percent of brain injuries that stem from firearms, the patient dies. Of the lucky 1 in 10, virtually all are thought to live with persistent disabilities.

In the last 15 years, however, better treatments have greatly improved the odds of survival. "In Iraq, we were fooled many times," said Duke University neurosurgeon Gerald Grant, who was an Air Force physician at Joint Base Balad in that country. Patients whose scans showed that shrapnel had crossed between the brain's hemispheres or cut a wide swath of destruction - injuries long thought to be a swift sentence of death - would often live.

But the result, as Giffords may yet show, is almost always a person profoundly changed by the injury.

As many as half of those who have had penetrating brain injury will suffer epileptic seizures and will have a higher risk of them for the rest of their lives, experts say.

Because these injuries often leave a victim fully conscious during and immediately after, many will retain vivid memories of the horror and suffer flashbacks, nightmares, anxiety and withdrawal, the hallmarks of post-traumatic stress disorder.

Vietnam veterans with a penetrating brain injury have shown steeper cognitive decline than that of their uninjured peers - apparently an accelerated version of normal age-related decline.

Beyond those broad strokes, the exact consequences of a penetrating brain injury depend heavily on where and at what speed the foreign body penetrated the skull.

"There are some parts of the brain that have high real estate value," says Dr. Jam Ghajar, president of the Brain Trauma Foundation and clinical professor of neurological surgery at Weill Cornell Medical College in New York City. "If you go into the brainstem, or a millimeter to the right or left, you can have massive disruption and almost certain death. You go into the frontal lobe and you have a lot more room for error."

The brain is a marvel of redundancy, parallel networks and interlocking message centers that might, with time, rewire around obstacles. But many clusters have precise functions - governing word access or face recognition, or processing vision, hearing and smell. Damage to those can cause specific, maybe permanent, impairments.

Damage to deep brain structures such as the amygdala or the hypothalamus will likely disturb a victim's ability to fully form, retain and retrieve memories that are freighted with emotion. Such impairments can wreak havoc on relationships and day-to-day functioning.

Some damage is subtler still. When a penetrating object has stretched or torn some tissue, including the connective "white matter" that forms bridges among brain regions, problems of attention, memory and social processing make it tough to navigate the demands of work, high-level thinking or new social situations.

Damage to the frontal lobes - common in traumatic brain injury because they lie right behind the forehead - can disturb a person's ability to formulate plans, read or respond to social cues, and suppress the impulse to do or say things that might be socially inappropriate.

Such impairments - labored speech, flat emotion, an odd social manner, an inability to make and carry out a plan - often linger. Those symptoms plague many of the estimated 5.3 million Americans who live with the persistent consequences of brain trauma. Little wonder that brain injury is often called the silent epidemic.

After the threat of death has passed, the challenge of regaining lost abilities - and of adjusting to life without others - is where the power of human resilience and inventiveness really inspires awe and humility, say those who have studied such injuries or witnessed the fallout up close.

"It's been a heartbreaking and inspiring thing to see," said Daniel Gross, whose younger brother Matthew, 41, was shot through the head 14 years ago by a gunman on the observation deck of New York's Empire State Building. After a week in a coma, Matthew first struggled to piece sentences together. Fully articulate after years of rehabilitation, he wrestles now with more subtle conventions of tactful conversation - the result of the bullet's passage through the frontal lobes on both sides of his brain.

Jordan Grafman, an expert on the long-term effects of penetrating trauma, says the survivors he has studied are remarkable not only for having survived but also for their determination to adapt and grow beyond their losses.

"At least half of our guys are working in full-time jobs and have families," says Grafman, director of research on brain injury at the Kessler Foundation in West Orange, N.J. "While people are uniformly left with impairments that are significant, they often show a tremendous ability to recover and really live productive and meaningful lives."

A patient's long-term recovery is profoundly affected by the person he or she was before the injury, Grafman says: A person who was clever, socially adept and intellectually engaged before the injury is likely to recover more lost capability than a person who had less mental horsepower or fewer social resources - friends, school, work, hobbies.

Grafman's conclusion comes from a unique cache of data: a decades-long study that has tracked some 200 Vietnam veterans who survived penetrating brain injury. The military's practice of testing troops for mental fitness gave researchers a standard gauge of intelligence and ability on each person that predated his injury. That provided a basis for measuring changes in a survivor's cognitive function in the decades after.

Ingoing scores on the armed forces' qualifying test have been the best predictor of a brain injury survivor's recovery from impairment, Grafman says. Now the study has begun to assess the influence of caregivers' styles - whether they are demanding or lenient, pushy or reserved, socially linked or more withdrawn.

Ironically, for those best equipped to rebuild their lives - people who, pre-injury, were exceptionally bright and highly motivated - the injury can pack a cruel surprise. Many grasp the extent of their impairments and are impatient to regain lost abilities that may never come back or that return at an agonizing snail's pace. Such survivors, Grafman says, are more vulnerable to depression and anxiety, which can impede progress and make life a misery.

As the nation tracks the recovery of Giffords, some worry about how the weight of expectations - and the Arizona Democrat's own formidable intelligence and drive - will affect her ability to overcome or adapt to the impairments likely to come with her injury.

One of them is Jackie Nink Pflug, who survived a bullet to her head at point-blank range during the 1985 hijacking of an EgyptAir flight from Athens to Cairo.

During years of painstaking recovery, Pflug relearned how to find her words, read a book, count money and navigate the world with seizures, excruciating headaches, a narrow field of vision, unreliable memory and the loss of hearing in one ear.

Asked what she would tell Giffords, Pflug urges her, above all, to "be patient with yourself."

In the first several years, she says, she sometimes "didn't know where the brain injury ended and the depression began." But rather than slow down, she pushed harder. "I wanted to do better, and my brain wasn't always ready for it."

Now, she says, "I'm just really good to myself." Giffords should be too, she adds.

"Even the littlest things, have a party about it."

(c) 2011, Los Angeles Times.
Distributed by McClatchy-Tribune Information Services.

Teen brains over-process rewards, suggesting root of risky behavior, mental ills

2011-01-27T07:31:00.000-08:00

Teen brains over-process rewards, suggesting root of risky behavior, mental ills
January 26th, 2011 in Medicine & Health / Neuroscience

Each row represents the activity in a neuron at key times during the task. At the time of reward, nearly one-third of adolescent neurons became excited (shown in red) though the level of inhibition (in blue) changed marginally. Adult neurons registered much higher inhibitory activity and less excitation. Credit: B. Moghaddam

University of Pittsburgh researchers have recorded neuron activity in adolescent rat brains that could reveal the biological root of the teenage propensity to consider rewards over consequences and explain why adolescents are more vulnerable to drug addiction, behavioral disorders, and other psychological ills.

The team reports in the Journal of Neuroscience that electrode recordings of adult and adolescent brain-cell activity during the performance of a reward-driven task show that adolescent brains react to rewards with far greater excitement than adult brains. This frenzy of stimulation occurred with varying intensity throughout the study along with a greater degree of disorganization in adolescent brains. The brains of adult rats, on the other hand, processed their prizes with a consistent balance of excitation and inhibition.

The extreme difference in brain activity provides a possible physiological explanation as to why teenagers are more prone than adults to rash behavior, addiction, and mental diseases, said lead researcher Bita Moghaddam, a professor of neuroscience in Pitt's School of Arts and Sciences. She and coauthor David Sturman, a Pitt neuroscience doctoral student, observed the disparate reactions to reward in individual neurons in the orbitofrontal cortex, a brain region that weighs payoff and punishment to plan and make decisions.

"The disorganized and excess excitatory activity we saw in this part of the brain means that reward and other stimuli are processed differently by adolescents," Moghaddam said. "This could intensify the effect of reward on decision making and answer several questions regarding adolescent behavior, from their greater susceptibility to substance abuse to their more extreme reactions to pleasurable and upsetting experiences."

In addition, malfunctions in the orbitofrontal cortex have been observed in cases of schizophrenia, mood disorders, and other psychological disturbances, Moghaddam said. The type of erratic activity in the cortex that she and Sturman observed could aggravate these conditions at a time when the maturing brain is vulnerable.

"The symptoms of these illnesses generally begin to appear during adolescence," Moghaddam said. "Adolescence is a period of behavioral and psychiatric vulnerabilities, so the disorganized brain activity and excess excitation could push a brain already predisposed to mental disorders too far, triggering the onset of symptoms."

Adult and adolescent neural activity was similar at first. When a reward was expected (sessions 3-6), adolescent brain activity spiked, followed by a slow decrease after the sugar pellet was received (food trough entry). Adults experienced a similar rapid increase in activity followed by a quick return to baseline. Credit: B. Moghaddam

The study is the first to record and compare individual neuron activity in adult and adolescent brains during the performance of a task. Moghaddam and Sturman presented adult and adolescent rats—which exhibit behavioral and biological similarities to adult and teenage humans—with three holes to poke their noses through; the rats each received a sugar pellet when they chose the center hole.
Brain activity in the adolescents was similar to that of the adults most of the time but striking differences arose when the younger rats retrieved rewards. As each of the adult rats collected a sugar pellet, the orbitofrontal cortex neurons showed the normal increase in both excitation and inhibition, with consistent levels of each impulse throughout the study.

Adolescents, on the other hand, exhibited surges of excitation that ranged from twice to four times the levels in adults. At the same time, the inhibitory impulses in the adolescents' brains barely changed from the low levels they experienced before receiving the sugar pellet.

Provided by University of Pittsburgh

Out of mind in a matter of seconds: How fast neuronal networks delete sensory information

2011-01-24T19:12:00.000-08:00

Out of mind in a matter of seconds: How fast neuronal networks delete sensory information
January 24th, 2011 in Physics / General Physics
An activity pattern is comparable to a communication protocol. It indicates which neuron is active at a given time. Credit: MPI for Dynamics and Selforganisatio. The dynamics behind signal transmission in the brain are extremely chaotic. This conclusion has been reached by scientists from the Max Planck Institute for Dynamics and Self-Organization at the University of Gottingen. In addition, the researchers calculated, for the first time, how quickly information stored in the activity patterns of the cerebral cortex neurons is discarded. At one bit per active neuron per second, the speed at which this information is forgotten is surprisingly high.

The brain codes information in the form of electrical pulses, known as spikes. Each of the brain’s approximately 100 billion interconnected neurons acts as both a receiver and transmitter: these bundle all incoming electrical pulses and, under certain circumstances, forward a pulse of their own to their neighbours. In this way, each piece of information processed by the brain generates its own activity pattern. This indicates which neuron sent an impulse to its neighbours: in other words, which neuron was active, and when. Therefore, the activity pattern is a kind of communication protocol that records the exchange of information between neurons.

How reliable is such a pattern? Do even minor changes in the neuronal communication produce a completely different pattern in the same way that a modification to a single contribution in a conversation could alter the message completely? Such behaviour is defined by scientists as chaotic. In this case, the dynamic processes in the brain could not be predicted for long. In addition, the information stored in the activity pattern would be gradually lost as a result of small errors. As opposed to this, so-called stable, that is non-chaotic, dynamics would be far less error-prone. The behaviour of individual neurons would then have little or no influence on the overall picture.

The new results obtained by the scientists in Göttingen have revealed that the processes in the cerebral cortex, the brain’s main switching centre, are extremely chaotic. The fact that the researchers used a realistic model of the neurons in their calculations for the first time was crucial. When a spike enters a neuron, an additional electric potential forms on its cell membrane. The neuron only becomes active when this potential exceeds a critical value. "This process is very important", says Fred Wolf, head of the Theoretical Neurophysics research group at the Max Planck Institute for Dynamics and Self-Organization. "This is the only way that the uncertainty as to when a neuron becomes active can be taken into account precisely in the calculations".

Older models described the neurons in a very simplified form and did not take into account exactly how and under what conditions a spike arises. "This gave rise to stable dynamics in some cases but non-stable dynamics in others", explains Michael Monteforte from the Max Planck Institute for Dynamics and Self-Organization, who is also a doctoral student at the Göttingen Graduate School for Neurosciences and Molecular Biosciences (GGNB). It was thus impossible to resolve the long-established disagreement as to whether the processes in the cerebral cortex are chaotic or not, using these models.

Thanks to their more differentiated approach, the Gottingen-based researchers were able to calculate, for the first time, how quickly an activity pattern is lost through tiny changes; in other words, how it is forgotten. Approximately one bit of information disappears per active neuron per second. "This extraordinarily high deletion rate came as a huge surprise to us", says Wolf. It appears that information is lost in the brain as quickly as it can be "delivered" from the senses.

This has fundamental consequences for our understanding of the neural code of the cerebral cortex. Due to the high deletion rate, information about sensory input signals can only be maintained for a few spikes. These new findings therefore indicate that the dynamics of the cerebral cortex are specifically tailored to the processing of brief snapshots of the outside world.

More information: Physical Review Letters, 105, 268104 (2010).

Provided by Max-Planck-Gesellschaft

Musicians' brains keep time--With one another

2011-01-20T19:05:00.000-08:00

Musicians' brains keep time--With one another
By Jordan Lite | Mar 16, 2009 08:01 PM

Ever wonder how musicians manage to play in unison? Credit their brain waves: they synchronize before and while musicians play a composition, according to new research.

German scientists report in BMC Neuroscience that they measured the brain waves of eight pairs of guitarists using electroencephalography (EEG) while they played a modern jazz piece called "Fusion #1" (by Alexander Buck). The researchers found that the guitarists' brain waves were aligned most during three pivotal times: when they were syncing up with a metronome, when they began playing the piece and at points during the composition that demanded the most synchrony.

The synchrony was most prominent in the frontal and central parts of the brain that regulate motor function. "Whenever synchrony of behavior was high, synchrony of brain waves were also high," Ulman Lindenberger, a director the Max Planck Institute for Human Development in Berlin, tells ScientificAmerican.com. But, "we can't assign a causal role to that synchronizing."

While brain synchrony during a duet seems like a given, it's a mystery how it happens, says Lindenberger, a psychologist. "One could speculate that this may be related to mirror neurons, the capacity of primates and humans to imagine the action of the other person while performing actions yourself," he says. "The mirror neuron system could be active during synchronized guitar playing."

Lindenberger says that inter-brain synchrony may also help explain humans' ability to engage in a host of other activities and behaviors that involve couples or teams, such as dancing, boxing, tennis and mother–child bonding. "People have an extraordinary capacity to synchronize their actions," he says. "When two people concentrate on the same thing, gestures and head movements are highly coordinated and supported by brain synchronicity. We think what we are getting through music has wider implications and social bonding behaviors are part of those wider implications."

The more you know a place, the more likely your memory will play spatial tricks

2011-01-18T06:35:00.000-08:00

The more you know a place, the more likely your memory will play spatial tricks
January 17th, 2011 in Medicine & Health / Psychology & Psychiatry

Using Northwestern University students, a new study shows that as students better understand the relationship between buildings on a campus, for example, over time memory biases cause them to exaggerate the distance between the north and south ends of campus.

Many suburbanites remember a time when they were once city dwellers. For a time many returned to the city for dining, cultural and entertainment purposes. But over time the suburbs and "the city" seemed much farther apart thereby resulting in less frequent trips.

A new Northwestern University study is the first to show that something may be happening cognitively that leads people to gradually become more biased, and at the same time more accurate, when it comes to their spatial memory as they become more familiar with a particular area.

In other words, as people better understand the relationship between buildings on a campus, for example, over time memory biases cause them to exaggerate the distance between the north and south ends of campus. They become more and more biased and see the boundaries of campus as being much farther apart.

David Uttal, professor of psychology in the Weinberg College of Arts and Sciences, along with colleague Alinda Friedman at the University of Alberta, are lead authors of the study. They witnessed firsthand how this plays out among students on the Northwestern campus.

“I’ve had students tell me that they may be a few minutes late for class because they are coming all the way from south campus,” Uttal said. “And I’m thinking, ‘It’s only a six-minute walk.’

“Another time I overheard a student say, ‘This better be good, because I don’t go to north campus for nothing.’

“That really intrigued me because if you look at a map it’s not at all clear where these divisions are,” said Uttal. “There are north and south ends of campus but treating it like a really sharp division, like a foreign world, it’s not justified based solely on geography. I think there is something really interesting going on here cognitively.”

There have been other studies demonstrating the existence of spatial biases and how they affect spatial judgments, but Uttal said there were never studies about how such biases developed and how they were learned.

By studying Northwestern freshmen over three quarters and comparing them to seniors, Uttal said two significant findings emerged.

First, Uttal said, “We can get simultaneously more accurate and more biased at the same time, which seems counterintuitive, but it really shows how different kinds of information are stored and thought about differently in the mind.”

Secondly, Uttal and his colleagues were able to establish a time-course for when these biases develop, concluding that when people are new to an area, they are not inherently biased. They develop biases as they become more familiar with their surroundings.

However, it is still unclear how people acquire information that lead to such biases.

“Part of it has to be somewhat cultural – so as you become more part of a group, a ‘northsider’ or ‘southsider’ if you will, you hear more about these distinctions,” Uttal said. “It’s also kind of an interaction between what you learn from other people and what you learn on your own.”

Uttal said the study’s findings have implications for both the Northwestern University community and society at large.

“One of the goals of our campus is to bring people closer together and establish community,” he said. “However, it is possible that people's cognitive biases could actually make this hard. If people start to think of different areas on campus as being farther apart as they get more involved in Northwestern, then it might actually be harder to get people to think about ‘One Northwestern’ the longer they are here.”

In addition, the study’s findings may have desegregation implications.

“As other researchers have shown, in segregated areas, people may tend to believe that they are farther apart than they really are,” Uttal said. “And if we’re trying to bring people together, we have to address the cognitive biases that they create. You tend to see the area that you’re close to as closer and the areas that are socially and cognitively further from you as being geographically farther. “

“Learning Fine-grained and Category Information in Navigable Real-World Space” was published in the journal Memory & Cognition in December. The study’s co-authors, in addition to Uttal and Friedman, are Linda Liu Hand and Christopher Warren, Northwestern University.

Provided by Northwestern University

Neuroscientists explain 'Proustian effect' of small details attached to big memories

2011-01-14T05:51:00.001-08:00

Neuroscientists explain 'Proustian effect' of small details attached to big memories
January 13th, 2011 in Medicine & Health / Neuroscience

Neuroscientists at MIT's Picower Institute of Learning and Memory have uncovered why relatively minor details of an episode are sometimes inexplicably linked to long-term memories. The work is slated to appear in the Jan. 13 issue of Neuron.

"Our finding explains, at least partially, why seemingly irrelevant information like the color of the shirt of an important person is remembered as vividly as more significant information such as the person's impressive remark when you recall an episode of meeting this person," said co-author Susumu Tonegawa, Picower Professor of Biology and Neuroscience and director of the RIKEN-MIT Center for Neural Circuit Genetics.

The data also showed that irrelevant information that follows the relevant event rather than precedes it is more likely to be integrated into long-term memory.

Shaping a memory

One theory holds that memory traces or fragments are distributed throughout the brain as biophysical or biochemical changes called engrams. The exact mechanism underlying engrams is not well understood.

MIT neuroscientists Arvind Govindarajan, assistant director of the RIKEN/MIT Center for Neural Circuit Genetics; Picower Institute postdoctoral associate Inbal Israely; and technical associate Shu-Ying Huang; and Tonegawa looked at single neurons to explore how memories are created and stored in the brain.

Previous research has focused on the role of synapses葉he connections through which neurons communicate. An individual synapse is thought to be the minimum unit necessary to establish a memory engram.

Instead of looking at individual synapses, the MIT study explored neurons' branch-like networks of dendrites and the multiple synapses within them.

Boosting the signal

Neurons sprout dendrites that transmit incoming electrochemical stimulation to the trunk-like cell body. Synapses located at various points act as signal amplifiers for the dendrites, which play a critical role in integrating synaptic inputs and determining the extent to which the neuron acts on incoming signals.

In response to external stimuli, dendritic spines in the cerebral cortex undergo structural remodeling, getting larger in response to repeated activity within the brain. This remodeling is thought to underlie learning and memory.

The MIT researchers found that a memory of a seemingly irrelevant detail葉he kind of detail that would normally be relegated to a short-term memory--may accompany a long-term memory if two synapses on a single dendritic arbor are stimulated within an hour and a half of each other.

"A synapse that received a weak stimulation, the kind that would normally accompany a short-term memory, will express a correlate of a long-term memory if two synapses on a single dendritic branch were involved in a similar time frame," Govindarajan said.

This occurs because the weakly stimulated synapse can steal or hitchhike on a set of proteins synthesized at or near the strongly stimulated synapse. These proteins are necessary for the enlargement of a dendritic spine that allows the establishment of a long-term memory.

"Not all irrelevant information is recalled, because some of it did not stimulate the synapses of the dendritic branch that happens to contain the strongly stimulated synapse," Israely said.

More information: "The dendritic branch is the preferred integrative unit for protein synthesis-dependent LTP," by Arvind Govindarajan, Inbal Israely, Shu-Ying Huang and Susumu Tonegawa. Neuron, 13 January, 2011.

Provided by Massachusetts Institute of Technology

Research shows emotional stress can change brain function

2011-01-13T07:17:00.000-08:00

Research shows emotional stress can change brain function
January 12th, 2011 in Medicine & Health / Neuroscience

Research conducted by Iaroslav Savtchouk, a graduate student, and S. June Liu, PhD, Associate Professor of Cell Biology and Anatomy at LSU Health Sciences Center New Orleans, has shown that a single exposure to acute stress affected information processing in the cerebellum – the area of the brain responsible for motor control and movement coordination and also involved in learning and memory formation. The work is published in the January 12, 2011 issue of The Journal of Neuroscience.

The researchers found that a five-minute exposure to the odor of a predator produced the insertion of receptors containing GluR2 at the connections (synapses) between nerve cells in the brain. GluR2 is a subunit of a receptor in the central nervous system that regulates the transfer of electrical impulses between nerve cells, or neurons. The presence of GluR2 changed electrical currents in the cerebellum in a way that increased activity and altered the output of the cerebellar circuit in the brains of mice.

Our ability to learn from experience and to adapt to our environment depends upon synaptic plasticity – the ability of a neuron or synapse to change its internal parameters in response to its history. A change in the GluR2 receptor subunit has been observed both during normal learning and memory as well as during many pathological processes, including drug addiction, stress, epilepsy, and ischemic stroke. However, the effect of this change on neuronal function is not fully understood.

"Our results lead to the testable prediction that emotional stress could affect motor coordination and other cerebellum-dependent cognitive functions," notes Dr. Liu. "These results are also applicable to communication in other brain regions and circuits. A long term goal is to alleviate the burden of neurological disorders such as motor dysfunctions, drug addiction, PTSD, and stroke."

Next steps include further research to improve our understanding of the role GluR2 insertion plays in normal learning and functioning of the brain, why some neurons contain GluR2-lacking receptors, but not others, and how that affects their role in brain function.

Provided by Louisiana State University

Babies process language in a grown-up way.

2011-01-08T06:24:00.000-08:00

Babies process language in a grown-up way
January 7th, 2011 in Medicine & Health / Neuroscience

This graphic shows estimated brain activity (indicated by bright colors) in four infants. Credit: UC San Diego School of Medicine

Babies, even those too young to talk, can understand many of the words that adults are saying – and their brains process them in a grown-up way.

Combining the cutting-edge technologies of MRI and MEG, scientists at the University of California, San Diego show that babies just over a year old process words they hear with the same brain structures as adults, and in the same amount of time. Moreover, the researchers found that babies were not merely processing the words as sounds, but were capable of grasping their meaning.

This study was jointly led by Eric Halgren, PhD, professor of radiology in the School of Medicine, Jeff Elman, PhD, professor of cognitive science in the Division of Social Sciences, and first author, Katherine E. Travis, of the Department of Neurosciences and the Multimodal Imaging Laboratory, all at UC San Diego. The work is published this week in the Oxford University Press journal Cerebral Cortex.

"Babies are using the same brain mechanisms as adults to access the meaning of words from what is thought to be a mental 'database' of meanings, a database which is continually being updated right into adulthood," said Travis.

Previously, many people thought infants might use an entirely different mechanism for learning words, and that learning began primitively and evolved into the process used by adults. Determining the areas of the brain responsible for learning language, however, has been hampered by a lack of evidence showing where language is processed in the developing brain.

While lesions in two areas called Broca's and Wernicke's (frontotemporal) areas have long been known to be associated with loss of language skills in adults, such lesions in early childhood have little impact on language development. To explain this discordance, some have proposed that the right hemisphere and inferior frontal regions are initially critical for language, and that classical language areas of adulthood become dominant only with increasing linguistic experience. Alternatively, other theories have suggested that the plasticity of an infant's brain allows other regions to take over language-learning tasks if left frontotemporal regions are damaged at an early age.

In addition to studying effects of brain deficits, language systems can be determined by identifying activation of different cortical areas in response to stimuli. In order to determine if infants use the same functional networks as adults to process word meaning, the researchers used MEG – an imaging process that measures tiny magnetic fields emitted by neurons in the brain – and MRI to noninvasively estimate brain activity in 12 to 18-month old infants.

In the first experiment, the infants listened to words accompanied by sounds with similar acoustic properties, but no meaning, in order to determine if they were capable of distinguishing between the two. In the second phase, the researchers tested whether the babies were capable of understanding the meaning of these words. For this experiment, babies saw pictures of familiar objects and then heard words that were either matched or mismatched to the name of the object: a picture of a ball followed by the spoken word ball, versus a picture of a ball followed by the spoken word dog.

Brain activity indicated that the infants were capable of detecting the mismatch between a word and a picture, as shown by the amplitude of brain activity. The "mismatched," or incongruous, words evoked a characteristic brain response located in the same left frontotemporal areas known to process word meaning in the adult brain. The tests were repeated in adults to confirm that the same incongruous picture/word combinations presented to babies would evoke larger responses in left frontotemporal areas.

"Our study shows that the neural machinery used by adults to understand words is already functional when words are first being learned," said Halgren, "This basic process seems to embody the process whereby words are understood, as well as the context for learning new words." The researchers say their results have implications for future studies, for example development of diagnostic tests based on brain imaging which could indicate whether a baby has healthy word understanding even before speaking, enabling early screening for language disabilities or autism.

Provided by University of California - San Diego

Gesturing while talking helps change your thoughts

2011-01-06T06:04:00.000-08:00

Gesturing while talking helps change your thoughts
January 5th, 2011 in Medicine & Health / Psychology & Psychiatry

Sometimes it's almost impossible to talk without using your hands. These gestures seem to be important to how we think. They provide a visual clue to our thoughts and, a new theory suggests, may even change our thoughts by grounding them in action.

University of Chicago psychological scientists Sian Beilock and Susan Goldin-Meadow are bringing together two lines of research: Beilock's work on how action affects thought and Goldin-Meadow's work on gesture. After a chat at a conference instigated by Ed Diener, the founding editor of Perspectives on Psychological Science, they designed a study together to look at how gesture affects thought.

For the study, published in Psychological Science, a journal of the Association for Psychological Science, Beilock and Goldin-Meadow had volunteers solve a problem known as the Tower of Hanoi. It's a game in which you have to move stacked disks from one peg to another. After they finished, the volunteers were taken into another room and asked to explain how they did it. (This is virtually impossible to explain without using your hands.) Then the volunteers tried the task again. But there was a trick: For some people, the weight of the disks had secretly changed, such that the smallest disk, which used to be light enough to move with one hand, now needed two hands.

People who had used one hand in their gestures when talking about moving the small disk were in trouble when that disk got heavier. They took longer to complete the task than did people who used two hands in their gestures—and the more one-handed gestures they used, the longer they took. This shows that how you gesture affects how you think; Goldin-Meadow and Beilock suggest that the volunteers had cemented how to solve the puzzle in their heads by gesturing about it (and were thrown off by the invisible change in the game).

In another version of the experiment, published in Perspectives in Psychological Science, the volunteers were not asked to explain their solution; instead, they solved the puzzle a second time before the disk weights were changed. But moving the disks didn't affect performance in the way that gesturing about the disks did. The people who gestured did worse after the disk weights switched, but the people who moved the disks did not—they did just as well as before. "Gesture is a special case of action. You might think it would have less effect because it does not have a direct impact on the world," says Goldin-Meadow. But she and Beilock think it may actually be having a stronger effect, "because gesturing about an act requires you to represent that act." You aren't just reaching out and handling the thing you're talking about; you have to abstract from it, indicating it by a movement of your hands.

In the article published in Perspectives in Psychological Science, the two authors review the research on action, gesture, and thought. Gestures make thought concrete, bringing movement to the activity that's going on in your mind.

This could be useful in education; Goldin-Meadow and Beilock have been working on helping children to understand abstract concepts in mathematics, physics, and chemistry by using gesture. "When you're talking about angular momentum and torque, you're talking about concepts that have to do with action," Beilock says. "I'm really interested in whether getting kids to experience some of these actions or gesture about them might change the brain processes they use to understand these concepts." But even in math where the concepts have little to do with action, gesturing helps children learn—maybe because the gestures themselves are grounded in action.

Provided by Association for Psychological Science

In Brief: The cocktail party problem

2011-01-05T05:00:00.000-08:00

In Brief: The cocktail party problem
January 4th, 2011 in Medicine & Health / Research

People can identify a repeating sound in a noisy room, but only when the noise includes mixtures of distinct distracting sounds, according to a study published this week in the Proceedings of the National Academy of Sciences.

Sound researchers have pondered this so-called "cocktail party problem," which underlies the ability to focus on a specific, unfamiliar sound.

To determine how the auditory system parses sound seemingly effortlessly, Josh H. McDermott and colleagues presented listeners with a synthesized audio recording that resembled everyday sounds, such as spoken words and animal vocalizations.

When the target sound was presented with one other sound, the listeners heard the mixture as a single sound and were unable to identify the target correctly.

However, when the target sound was presented repeatedly, mixed with a distinct distracting sound each time, the listeners developed an impression of the repeating target and identified it in the mixtures.

Further, the listeners' ability to recognize the target sound depended on the number of different mixtures in the audio recording, not the number of times the target was presented.

Hence, the authors suggest, the auditory system detects sounds based on patterns of time and frequency, such as might be produced by feet pounding on pavement or by branches swaying in the wind, and interprets the patterns as sound sources.

More information: "Recovering sound sources from embedded repetition," by Josh H. McDermott, David Wrobleski, and Andrew J. Oxenham, Proceedings of the National Academy of Sciences, January 2010.

Provided by Proceedings of the National Academy of Sciences

Tempo Rubato: Animacy Speeds Up Time in the Brain

2011-01-01T06:06:00.000-08:00

Tempo Rubato: Animacy Speeds Up Time in the Brain

Mauro Carrozzo 1,2, Alessandro Moscatelli 2, Francesco Lacquaniti 2,3,4

1 Institute of Neuroscience, National Research Council, Rome, Italy,
2 Laboratory of Neuromotor Physiology, Santa Lucia Foundation, Rome, Italy,
3 Centre of Space BioMedicine, University of Rome Tor Vergata, Rome, Italy,
4 Department of Neuroscience, University of Rome Tor Vergata, Rome, Italy

Abstract
Background
How do we estimate time when watching an action? The idea that events are timed by a centralized clock has recently been called into question in favour of distributed, specialized mechanisms. Here we provide evidence for a critical specialization: animate and inanimate events are separately timed by humans.

Methodology/Principal Findings
In different experiments, observers were asked to intercept a moving target or to discriminate the duration of a stationary flash while viewing different scenes. Time estimates were systematically shorter in the sessions involving human characters moving in the scene than in those involving inanimate moving characters. Remarkably, the animate/inanimate context also affected randomly intermingled trials which always depicted the same still character.

Conclusions/Significance
The existence of distinct time bases for animate and inanimate events might be related to the partial segregation of the neural networks processing these two categories of objects, and could enhance our ability to predict critically timed actions.

Uncovering the neurobiological basis of general anesthesia

2010-12-31T05:15:00.000-08:00

Uncovering the neurobiological basis of general anesthesia
December 30th, 2010 in Medicine & Health / Research

The use of general anesthesia is a routine part of surgical operations at hospitals and medical facilities around the world, but the precise biological mechanisms that underlie anesthetic drugs' effects on the brain and the body are only beginning to be understood. A review article in the December 30 New England Journal of Medicine brings together for the first time information from a range of disciplines, including neuroscience and sleep medicine, to lay the groundwork for more comprehensive investigations of processes underlying general anesthesia.

"A key point of this article is to lay out a conceptual framework for understanding general anesthesia by discussing its relation to sleep and coma, something that has not been done in this way before," says Emery Brown, MD, PhD, of the Massachusetts General Hospital (MGH) Department of Anesthesia, Critical Care and Pain Medicine, lead author of the NEJM paper. "We started by stating the specific physiological states that comprise general anesthesia – unconsciousness, amnesia, lack of pain perception and lack of movement while stable cardiovascular, respiratory and thermoregulatory systems are maintained – another thing that has never been agreed upon in the literature; and then we looked at how it is similar to and different from the states that are most similar – sleep and coma."

After laying out their definition, Brown and his co-authors – Ralph Lydic, PhD, a sleep expert from the University of Michigan, and Nicholas Schiff, MD, an expert in coma from Weill Cornell Medical College – compare the physical signs and electroencephalogram (EEG) patterns of general anesthesia to those of sleep. While it is common to describe general anesthesia as going to sleep, there actually are significant differences between the states, with only the deepest stages of sleep being similar to the lightest phases of anesthesia induced by some types of agents.

While natural sleep normally cycles through a predictable series of phases, general anesthesia involves the patient being taken to and maintained at the phase most appropriate for the procedure, and the phases of general anesthesia at which surgery is performed are most similar to states of coma. "People have hesitated to compare general anesthesia to coma because the term sounds so harsh, but it really has to be that profound or how could you operate on someone?" Brown explains. "The key difference is this is a coma that is controlled by the anesthesiologist and from which patients will quickly and safely recover."

In detailing how different anesthetic agents act on different brain circuits, the authors point out some apparently contradictory information – some drugs like ketamine actually activate rather than suppress neural activity, an action that can cause hallucinations at lower doses. Ketamine blocks receptors for the excitatory transmitter glutamate, but since it has a preference for receptors on certain inhibitory neurons, it actually stimulates activity when it blocks those inhibitors. This excess brain activity generates unconsciousness through a process similar to what happens when disorganized data travels through an electronic communication line and blocks any coherent signal. A similar mechanism underlies seizure-induced unconsciousness.

Brown also notes that recent reports suggest an unexpected use for ketamine – to treat depression. Very low doses of the drug have rapidly reduced symptoms in chronically depressed patients who had not responded to traditional antidepressants. Ketamine is currently being studied to help bridge the first days after a patient begins a new antidepressant – a time when many may be at risk of suicide – and the drug's activating effects may be akin to those of electroconvulsive therapy.

Another unusual situation the authors describe is the case of a brain-injured patient in a minimally conscious state who actually recovered some functions through administration of the sleep-inducing drug zolpidem (Ambien). That patient's case, analyzed previously by Schiff, mirrors a common occurrence called paradoxical excitation, in which patients in the first stage of general anesthesia may move around or vocalize. The authors describe how zolpidem's suppression of the activity of a brain structure called the globus pallidus – which usually inhibits the thalamus – stimulates activity in the thalamus, which is a key neural control center. They hypothesize that a similar mechanism may underlie paradoxical excitation.

"Anesthesiologists know how to safely maintain their patients in the states of general anesthesia, but most are not familiar with the neural circuit mechanisms that allow them to carry out their life-sustaining work," Brown says. "The information we are presenting in this article – which includes new diagrams and tables that don't appear in any anesthesiology textbook – is essential to our ability to further understanding of general anesthesia, and this is the first of several major reports that we anticipate publishing in the coming year."

Schiff adds, "We think this is, conceptually, a very fresh look at phenomena we and others have noticed and studied in sleep, coma and use of general anesthesia. By reframing these phenomena in the context of common circuit mechanisms, we can make each of these states understandable and predictable."

Provided by Massachusetts General Hospital

Auditory cortex spatial sensitivity sharpens during task performance

2010-12-29T07:32:00.000-08:00

Auditory cortex spatial sensitivity sharpens during task performance

Chen-Chung Lee & John C Middlebrooks

Nature Neuroscience, Volume: 14, Pages: 108-114
Year published: (2011), Received 22 September 2010, Accepted 13 November 2010, Published online 12 December 2010
DOI:doi:10.1038/nn.2713

Abstract:
Activity in the primary auditory cortex (A1) is essential for normal sound localization behavior, but previous studies of the spatial sensitivity of neurons in A1 have found broad spatial tuning. We tested the hypothesis that spatial tuning sharpens when an animal engages in an auditory task. Cats performed a task that required evaluation of the locations of sounds and one that required active listening, but in which sound location was irrelevant. Some 26�44% of the units recorded in A1 showed substantially sharpened spatial tuning during the behavioral tasks as compared with idle conditions, with the greatest sharpening occurring during the location-relevant task. Spatial sharpening occurred on a scale of tens of seconds and could be replicated multiple times in ~1.5-h test sessions. Sharpening resulted primarily from increased suppression of responses to sounds at least-preferred locations. That and an observed increase in latencies suggest an important role of inhibitory mechanisms.

(a) Poststimulus time histogram (PSTH) showing activity as a function of time (horizontal axis) and head-centered stimulus location (vertical axis) for one example unit in A1 in the right hemisphere during the idle condition

Each symbol represents one unit, with the value in horizontal and vertical axes corresponding to its ERRF width in two different conditions. The symbols lying below the diagonal line represent units for which spatial tuning sharpened

Source: Nature Neuroscience
http://www.nature.com/neuro/journal/v14/n1/abs/nn.2713.html?lang=en

Scans could predict onset of schizophrenia

2010-12-24T07:01:00.000-08:00

Brain scans could be used to predict the onset of schizophrenia in young people with a family history of the disease, a new study suggests.

Abused, neglected children have lower IQ in teens

2010-12-23T06:55:00.000-08:00

Abused, neglected children have lower IQ in teens
December 22nd, 2010 in Medicine & Health / Health
University of Queensland research has found children who have been abused or neglected are likely to struggle academically during adolescence.
The research drew upon data from the Mater-University Study of Pregnancy (MUSP) – a longitudinal study of more than 7000 mothers and their children born at Brisbane's Mater Hospital from 1981-83.

Lead author and pediatrician Ryan Mills said the research involved confidentially linking allegations of maltreatment reported to the Department of Families, Youth and Community Care with the MUSP database.

“Both child abuse and child neglect are independently associated with impaired cognition and academic functioning in adolescence,” Dr. Mills said.

“These findings suggest that both abuse and neglect have independent and important adverse effects on a child's cognitive development.”

The MUSP database provided results of numeracy, literacy and abstract reasoning tests completed by 3796 adolescents at age 14.

The 298 adolescents (7.9 percent) who had been reported as victims of maltreatment scored the equivalent of approximately three IQ points lower than those who had not been maltreated, after accounting for a large range of socioeconomic and other factors.

Co-author Lane Strathearn, a UQ medical and PhD graduate now based at the Baylor College of Medicine and Texas Children's Hospital, said this study was one of the first to analyse outcomes of abuse and neglect independently.

“Studies have repeatedly demonstrated that at least half of maltreated children experience more than one type of abuse or neglect,” Dr. Strathearn said.

“Our sample was no different; 74 percent of the children reported to the state as suspected cases of neglect also had been reported as suspected victims of abuse.

“Our method involved grouping the physical, emotional and sexual abuse cases together and assessing both abuse and neglect - reported or substantiated - as independent nonexclusive predictor variables.”

The results highlighted the seriousness of child neglect, Dr. Strathearn said.

“The effects of abuse and neglect were found to be independent and quantitatively similar; children who experienced both abuse and neglect were doubly affected,” he said.

“The results support the notion that child neglect has developmental effects that are independently at least as deleterious as abuse, which has important implications for the allocation of resources into additional research into, and prevention of, child neglect.”

More information: Dr. Mills and Dr. Strathearn worked with a team of UQ colleagues, including Rosa Alati, Michael O'Callaghan, Jake Najman, Gail Williams and William Bor. The study was published online this month in medical journal Pediatrics.

Provided by University of Queensland

Brain imaging predicts future reading progress in children with dyslexia

2010-12-21T05:53:00.000-08:00

Brain imaging predicts future reading progress in children with dyslexia
December 20th, 2010 in Medicine & Health / Research

Brain scans of adolescents with dyslexia can be used to predict the future improvement of their reading skills with an accuracy rate of up to 90 percent, new research indicates. Advanced analyses of the brain activity images are significantly more accurate in driving predictions than standardized reading tests or any other measures of children's behavior.

The finding raises the possibility that a test one day could be developed to predict which individuals with dyslexia would most likely benefit from specific treatments.

The research was published Dec. 20, 2010, in the Proceedings of the National Academy of Science.

"This approach opens up a new vantage point on the question of how children with dyslexia differ from one another in ways that translate into meaningful differences two to three years down the line," Bruce McCandliss, Patricia and Rodes Hart Chair of Psychology and Human Development at Vanderbilt University's Peabody College and a co-author of the report, said. "Such insights may be crucial for new educational research on how to best meet the individual needs of struggling readers.

"This study takes an important step toward realizing the potential benefits of combining neuroscience and education research by showing how brain scanning measures are sensitive to individual differences that predict educationally relevant outcomes," he continued.

The research was primarily conducted at Stanford University and led by Fumiko Hoeft, associate director of neuroimaging applications at the Stanford University School of Medicine. In addition to McCandliss, Hoeft's collaborators included researchers at MIT, the University of Jyväskylä in Finland and the University of York in the United Kingdom.

"This finding provides insight into how certain individuals with dyslexia may compensate for reading difficulties," Alan E. Guttmacher, director of the National Institutes of Health's Eunice Kennedy Shriver National Institute of Child Health and Human Development, which provided funding for the study, said.

"Understanding the brain activity associated with compensation may lead to ways to help individuals with this capacity draw upon their strengths," he continued. "Similarly, learning why other individuals have difficulty compensating may lead to new treatments to help them overcome reading disability."

The researchers used two types of brain imaging technology to conduct their study. The first, functional magnetic resonance imaging (fMRI), depicts oxygen use by brain areas involved in a particular task or activity. The second, diffusion tensor magnetic resonance imaging (DTI), maps white matter tracts that are the brain's wiring, revealing connections between brain areas.

The 45 children who took part in the study ranged in age from 11 to 14 years old. Each child first took a battery of tests to determine their reading abilities. Based on these tests, the researchers classified 25 children as having dyslexia, which means that they exhibited significant difficulty learning to read despite having typical intelligence, vision and hearing and access to typical reading instruction.

During the fMRI scan, the youths were shown pairs of printed words and asked to identify pairs that rhymed, even though they might be spelled differently. The researchers investigated activity patterns in a brain area on the right side of the head, near the temple, known as the right inferior frontal gyrus, noting that some of the children with dyslexia activated this area much more than others. DTI scans of these same children revealed stronger connections in the right superior longitudinal fasciculus, a network of brain fibers linking the front and rear of brain.

When the researchers once again administered the reading test battery to the youths two and a half years later, they found that the 13 youths showing the stronger activation pattern in the right inferior frontal gyrus were much more likely to have compensated for their reading difficulty than were the remaining 12 youths with dyslexia. When they combined the most common forms of data analysis across the fMRI and DTI scans, they were able to predict the youths' outcomes years later with 72 percent accuracy.

The researchers then adapted algorithms used in artificial intelligence research to refine the brain activity data to create models that would predict the children's later progress. Using this relatively new technique, the researchers could use the brain scanning data collected at the beginning of the study to predict with over 90 percent accuracy which children would go on to improve their reading skills two and a half years later.

In contrast, the battery of standardized, paper-and-pencil tests typically used by reading specialists did not aid in predicting which of the children with dyslexia would go on to improve their reading ability years later.

"Our findings add to a body of studies looking at a wide range of conditions that suggest brain imaging can help determine when a treatment is likely to be effective or which patients are most susceptible to risks," Hoeft said.

Hoeft further explained that the largest improvement was seen in reading comprehension, which is the ultimate goal of reading. The youths showed less improvement in other reading-related skills such as phonological awareness. Typically developing readers tend to develop phonemic awareness skills before developing fluency and comprehension skills.

Hoeft suggested the finding that youths with dyslexia recruited right brain frontal regions to compensate for their reading difficulties, rather than regions in the left side of their brains, as typical readers do, may have something to do with this.

The study is part of a rapidly developing field of research known as "educational neuroscience" that brings together neuroimaging studies with educational research to understand how individual learners differ in brain structure and activity and how learning can drive changes at the neural level. Such questions are now being effectively examined in young children even before reading instruction begins, McCandliss explained in a Proceedings of the National Academy of Science article published earlier this year.

"This latest study provides a simple answer to a very complex question—'what can neuroscience contribute to complex issues in education?'" McCandliss said. "Here we have a clear example of how new insights and discoveries are beginning to emerge by pairing rigorous education research with novel neuroimaging approaches."

Provided by Vanderbilt University

Researchers discover new way to reduce anxiety, stress

2010-12-18T05:43:00.000-08:00

Researchers discover new way to reduce anxiety, stress
December 17th, 2010 in Medicine & Health / Neuroscience

Two North American researchers have made a major discovery that will benefit people who have anxiety disorders. Bill Colmers, a professor of pharmacology and researcher in the Faculty of Medicine & Dentistry at the University of Alberta, collaborated with Janice Urban, an associate professor in the department of physiology and biophysics at the Chicago Medical School at Rosalind Franklin University of Medicine and Science. The duo, who have been researching anxiety for five years, discovered that blocking a process in nerve cells reduces anxiety, meaning a new drug could now be developed to better treat anxiety disorders. Their findings were published in the peer-reviewed Journal of Neuroscience in December’s edition.

Colmers explained that current anxiety drugs on the market are non-selective, which means they inhibit various neurons, or nerve cells, in the brain—including ones you don’t want to inhibit. Because no one could pinpoint how to reduce anxiety, all kinds of neurons had to be treated with anxiety medication, which can have undesirable side-effects such as drowsiness.

But now drugs can now be designed to more specifically treat anxiety disorders, likely meaning fewer undesirable side effects and a better quality of life for those with anxiety. Anxiety disorders are the most common mental-health issue in the country, affecting one in 10 Canadian adults, according to the Anxiety Disorders Association of Canada.

For years, researchers have understood what processes in the brain are responsible for high and low anxiety levels, but no one had been able to identify what triggers this process.

“No one else has discovered this,” said Colmers, a senior scientist with funding from the Alberta Heritage Foundation for Medical Research (a provincial agency now called Alberta Innovates – Health Solutions). “Others have identified the behaviour, but now we know why this process happens and how it works. Now we know why certain chemical messengers behave the way they do.”

There are two chemical messengers in a specific part of the brain known to regulate anxiety. One messenger, known as neuropeptide Y, makes one less anxious while the other, known as corticotropin-releasing factor or CRF, makes one more anxious.

These two chemical messengers regulate how “excitable” the nerve cell gets. Neuropeptide Y causes nerve cells to be less active, meaning the cells will fire less. The other chemical messenger, CRF, causes cells to be more active and fire more often. The more often these neurons fire, the more anxious a person becomes.

By working with laboratory models, Colmers and Urban discovered that blocking the process responsible for regulating cell excitability triggers less anxiety. Blocking this process had the same effect as the chemical messenger neuropeptide Y, which makes people less anxious.

Colmers said it could be 10 years before patients could start taking a new drug for anxiety based on these research findings, but the find is still significant.

“There is a real need to find better treatments for anxiety—to better target the processes in the brain that trigger anxiety disorders.”

Provided by University of Alberta

Where unconscious memories form

2010-12-16T09:46:00.001-08:00

Where unconscious memories form
December 15th, 2010 in Medicine & Health / Neuroscience

A small area deep in the brain called the perirhinal cortex is critical for forming unconscious conceptual memories, researchers at the UC Davis Center for Mind and Brain have found.

The perirhinal cortex was thought to be involved, like the neighboring hippocampus, in "declarative" or conscious memories, but the new results show that the picture is more complex, said lead author Wei-chun Wang, a graduate student at UC Davis.

The results were published Dec. 9 in the journal Neuron.

We're all familiar with memories that rise from the unconscious mind. Imagine looking at a beach scene, said Wang. A little later, someone mentions surfing, and the beach scene pops back into your head.

Declarative memories, in contrast, are those where we recall being on that beach and watching that surf competition: "I remember being there."

Damage to a structure called the hippocampus affects such declarative "I remember" memories, but not conceptual memories, Wang said. Neuroscientists had previously thought the same was true for the perirhinal cortex, which is located immediately next to the hippocampus.

Wang and colleagues carried out memory tests on people diagnosed with amnesia, who had known damage to the perirhinal cortex or other brain areas. They also carried out functional magnetic resonance imaging (fMRI) scans of healthy volunteers while they performed memory tests.

In a typical test, they gave the subjects a long list of words, such as chair, table or spoon, and asked them to think about how pleasant they were.

Later, they asked the subjects to think up words in different categories, such as "furniture."

Amnesiacs with damage to the perirhinal cortex performed poorly on the tests, while the same brain area lit up in fMRI scans of the healthy control subjects.

The study helps us understand how memories are assembled in the brain and how different types of brain damage might impair memory, Wang said. For example, Alzheimer's disease often attacks the hippocampus and perirhinal cortex before other brain areas.

Provided by University of California - Davis

Extended Mind Redux: A Response

2010-12-15T18:54:00.000-08:00

Extended Mind Redux: A Response
By ANDY CLARK

Thanks to all who read and commented on my recent Stone post, “Out of Our Brains.” Lots of interesting, challenging, and important issues were raised, but I’d like to react very briefly to just a few recurring themes, and to add one important, and accidentally omitted, note of thanks.
The thanks (and see comment 73) are to professor David Chalmers. Dave was co-author of my original 1998 paper “The Extended Mind,” and is the sole author of a wonderful foreword to my 2008 book, “Supersizing the Mind.” Dave had a big hand in the original paper. Everyone who asked about the thin line between tools and extensions, or about the vexed question of extending the conscious mind, should read his recent forward, too.

Themewise, I was struck by the somewhat remarkable fact that about half the commentators thought the general line about extending the mind was plausible and even obvious, while about half thought it was implausible and perhaps even self-evidently false. In optimistic mode (which I mostly am) I take this as a good sign: as suggesting that there is indeed something worth thinking about here. If I were feeling less upbeat, I might take it as a sign that I just hadn’t made the thought clear enough. A couple of comments made me worry on that score, so a few clarifications seem in order.

I didn’t mean to downplay the pivotal role of the brain/body in human thought and reason. I can indeed survive the loss of my iPhone but not the loss of my brain! But as Dave Chalmers has pointed out, I can also survive the loss of my finger, the loss of a few neurons, or even the wholesale ablation of my visual cortex. It does not follow that e.g. my visual cortex, when all is up and running normally, does not constitute part of my cognitive apparatus. This reveals something important. It is only when you turn up the magnification, seeing the biological agent as herself a kind of grab-bag of distinct circuits and capacities, that the possibility of true cognitive extension even becomes visible. That possibility then takes shape as the possibility that some non-biological circuitry (connected by various forms of looping interaction to the biological core) might become sufficiently integral to some of my cognitive performances as to count as part of the machinery of mind and reason.

This talk of the machinery of mind is important. A few commentators rightly suggested that mind itself is probably not a “thing” hence not worth trying to locate. That is not to say — heaven forbid — that it is a non-material thing. Rather, it might be a bit like trying to locate the adorableness of a kitten. There is nothing magically non-physical about the kitten, but trying to fine-tune the location of the adorableness still seems like some kind of error or category mistake. In the case of mind, I think what we have is an intuitive sense of the kind of capacities that we are gesturing at when we speak of minds, and so we can then ask: where is the physical machinery that makes those capacities possible? It is the physical machinery of thought and reason that the extended mind story is meant to concern.

A couple of replies touched on what is really one of the philosophical hot potatoes here, which is the distinction between “mere” inputs to a cognitive system and elements of the system itself. Critics of the extended mind (for example, Fred Adams and Ken Aizawa, in their 2008 book called “The Bounds of Cognition”) think theorists of extended cognition are guilty of confusing inputs to the cognitive engine with stuff that is part of (and “constitutes”) the cognitive engine. I think this distinction between “mere” inputs and processing elements in far less clear than it sounds. An analogy I sometimes use is with the workings of a turbo-driven car engine. Compare: the car makes exhaust fumes (outputs) that are also inputs that drive the turbo that adds power (up to around 30 percent more power) to the engine. The exhaust fumes are both outputs and self-generated inputs that, as they loop around, surely form a proper part of the overall power-generating mechanism. I think much the same is true of our use of bodily gestures while reasoning with others, and of the way that actively writing contributes to the process of thinking. The gestures and words on the page are outputs that immediately loop back in ways that form larger circuits of ongoing thinking and reasoning.

Some respondents raised important and interesting questions concerning conscious experience. I note only that my own account of cognitive extension is not meant to make any claims extending the machinery of consciousness beyond the brain. I myself am skeptical of such extensions. But some excellent philosophers (like Alva Noë in his 2009 book, “Out of Our Heads”) do go that far, and I would refer those interested in this issue to that short and accessible treatment.

Finally, special thanks to all those who suggested sci-fi books, or other stuff that I ought to be reading. My holiday stocking (and perhaps my mind) will be greatly expanded as a result.

Can't relax? It's all in your mind: Research shows stopping a thought puts more strain on the brain

2010-12-15T09:17:00.001-08:00

Can't relax? It's all in your mind: Research shows stopping a thought puts more strain on the brain
December 14th, 2010 in Medicine & Health / Neuroscience

Turns out, relaxing is exhausting—which could by why so many people struggle to unplug from work during vacation.

According to mathematicians at Case Western Reserve University, stopping a thought burns more energy than thinking-like stopping a truck on a downhill slope.

"Maybe this explains why it is so tiring to relax and think about nothing," says Daniela Calvetti, professor of mathematics and one of the authors of a new brain study published in an advanced online publication of the Journal of Cerebral Blood Flow & Metabolism.

Since opening up the brain for detailed monitoring isn't exactly practical, Calvetti teamed up with fellow mathematics professor Erkki Somersalo and Rossana Occhipinti, a postdoctoral researcher in physiology and biophysics, to create a computer model of brain metabolism.

Calvetti and Somersalo created a software package specifically designed to study the complex metabolic systems. The software-Metabolica-produces a numeric rendering of the pathways linking excitatory neurons that transmit thought or inhibitory neurons that put on the brakes with star-shaped brain cells called astrocytes. Astrocytes provide essential chemicals and functions to both kinds of neurons.

To stop a thought, the brain uses inhibitory neurons to prevent excitatory neurons from passing information-they block information by releasing gamma aminobutyric acid, commonly called GABA, which counteracts the effect of the neurotransmitter glutamate by excitatory neurons.

In other words, glutamate opens the synaptic gates and GABA holds them closed.

"The astrocytes, which are the Cinderellas of the brain, consume large amounts of oxygen mopping up and recycling the GABA and the glutamate, which is a neurotoxin," Somersalo says.

More oxygen requires more blood flow, although the connection between cerebral metabolism and hemodynamics is not fully understood yet.

All together, "It's a surprising expense to keep inhibition on," he says.

The researchers hope their work can provide some insight on brain diseases, which are often difficult to diagnose until advanced stages. Most brain maladies are linked to energy metabolism, and understanding the norm may enable doctors to detect problems earlier.

The toll inhibition takes may be particularly relevant to neurodegenerative diseases. "And that is truly exciting," Calvetti says.

Provided by Case Western Reserve University

Everyone thinks everyone else has less free will

2010-12-14T06:54:00.000-08:00

Everyone thinks everyone else has less free will
December 13th, 2010 in Medicine & Health / Psychology & Psychiatry
Generally, everyone seems to believe they have more free will than everyone else.

The subject of individual free will -- whether our fates are beyond our control or whether we command our own destinies -- has been hotly argued for centuries. Now scientists have revealed a new wrinkle in the debate: generally, everyone seems to believe they have more free will than everyone else.

Social psychologist Emily Pronin at Princeton University in New Jersey studies the differences between how we perceive ourselves and how we perceive others. According to her research, we tend to view our own judgment as sound but the judgment of others as irrational; recognize the biases in others but not ourselves; and see ourselves as more individualistic and others as more conformist.

Essentially, people judge others based on what they see. But they judge themselves based on what they think and feel, a difference that often leads to misunderstandings, disagreements and conflicts. Understanding the psychological basis of these differences might help relieve some of their negative consequences, Pronin suggested.

When Pronin began wondering about other consequences of this asymmetry, "beliefs in free will struck me as a key place to look, since those beliefs really matter for things like how much responsibility we assign to our own and others' actions," she said. In four experiments, Pronin and graduate student Matthew Kugler investigated how much people believed that their lives and those of their peers were guided by free will, findings they detailed online Dec. 13 in the Proceedings of the National Academy of Sciences.

In the first experiment, the researchers studied the most classic tenet of free will — the notion that one's actions cannot be determined in advance. Fifty college students were asked the rate on a scale of one to seven how predictable they thought certain past and future decisions in their lives and those of their roommates were, such as their choice of major in college or their ultimate career path. On average, the participants viewed their own pasts and futures as less predictable than their roommates by about one point on that scale.

"By the standards of psychological research, this is a large effect," Pronin said.

In the second and third experiments, 28 restaurant workers and 50 students were asked how many choices they thought were available in their futures and those of peers. The volunteers generally thought they had more pathways open to them, good and bad.

In the last experiment, 58 students created models predicting their own behavior and those of a roommate on a Saturday night or after finishing college that indicated how important personality, history, circumstances, intentions and desires were for outcomes. The volunteers saw their own future actions as most strongly driven by their intentions and desires instead of being predetermined by personality, history, or circumstances. In contrast, they viewed personality as the strongest predictor of their roommates' behavior.

"People have been debating about the existence of free will for ages," Pronin said. "Our research suggests one reason why this debate is so persistent -- people seem to have two views of free will. One view is when they look inwards and are convinced of their own free will; the other view is when they look outwards, at others, and are convinced that those others' actions could have been predicted in advance."

"This work is a terrific advance," said research psychologist Roy Baumeister at Florida State University in Tallahassee, who did not take part in this study. "Most debates about free will take an all-or-nothing form -- either everyone has it all the time, or nobody ever does."

As to why such a difference might have evolved, "when thinking about ourselves, it may be adaptive to believe that we can control what happens to us, and that belief requires thinking that we have free will," Pronin suggested. "When thinking about others, it may be adaptive to recognize the predictability in others' actions so that we can be prepared accordingly."

The scientists are intrigued by the consequences of these differing views on free will, as well as how they might vary across lifespan and different cultures.

"How does it impact beliefs about personal responsibility and guilt?" Pronin asked. "Are people likely to spend more time kicking themselves about things that went wrong in their past because they think they could have controlled those things, even though they wouldn't think this in the case of others?"

Provided by Inside Science News Service

Imaginar que comes ayuda a saciar el apetito

2010-12-11T05:13:00.002-08:00

Our brains are wired so we can better hear ourselves speak, study shows

2010-12-09T06:14:00.000-08:00

Activity in the auditory cortex when we speak and listen is amplified in some regions of the brain and muted in others. In this image, the black line represents muting activity when we speak. (Courtesy of Adeen Flinker)

Like the mute button on the TV remote control, our brains filter out unwanted noise so we can focus on what we're listening to. But when following our own speech, a new brain study from UC Berkeley shows that instead of one mute button, we have a network of volume settings that can selectively silence and amplify the sounds we make and hear.

Neuroscientists from UC Berkeley, UCSF and Johns Hopkins University tracked the electrical signals emitted from the brains of hospitalized epilepsy patients. They discovered that neurons in one part of the patients' hearing mechanism were dimmed when they talked, while neurons in other parts lit up.

Their findings, published today (Dec. 8, 2010) in the Journal of Neuroscience, offer new clues about how we hear ourselves above the noise of our surroundings and monitor what we say. Previous studies have shown a selective auditory system in monkeys that can amplify their self-produced mating, food and danger alert calls, but until this latest study, it was not clear how the human auditory system is wired.

"We used to think that the human auditory system is mostly suppressed during speech, but we found closely knit patches of cortex with very different sensitivities to our own speech that paint a more complicated picture," said Adeen Flinker, a doctoral student in neuroscience at UC Berkeley and lead author of the study.

"We found evidence of millions of neurons firing together every time you hear a sound right next to millions of neurons ignoring external sounds but firing together every time you speak," Flinker added. "Such a mosaic of responses could play an important role in how we are able to distinguish our own speech from that of others."

While the study doesn't specifically address why humans need to track their own speech so closely, Flinker theorizes that, among other things, tracking our own speech is important for language development, monitoring what we say and adjusting to various noise environments.

"Whether it's learning a new language or talking to friends in a noisy bar, we need to hear what we say and change our speech dynamically according to our needs and environment," Flinker said.

He noted that people with schizophrenia have trouble distinguishing their own internal voices from the voices of others, suggesting that they may lack this selective auditory mechanism. The findings may be helpful in better understanding some aspects of auditory hallucinations, he said.

Moreover, with the finding of sub-regions of brain cells each tasked with a different volume control job – and located just a few millimeters apart – the results pave the way for a more detailed mapping of the auditory cortex to guide brain surgery.

In addition to Flinker, the study's authors are Robert Knight, director of the Helen Wills Neuroscience Institute at UC Berkeley; neurosurgeons Edward Chang, Nicholas Barbaro and neurologist Heidi Kirsch of the University of California, San Francisco; and Nathan Crone, a neurologist at Johns Hopkins University in Maryland.

The auditory cortex is a region of the brain's temporal lobe that deals with sound. In hearing, the human ear converts vibrations into electrical signals that are sent to relay stations in the brain's auditory cortex where they are refined and processed. Language is mostly processed in the left hemisphere of the brain.

In the study, researchers examined the electrical activity in the healthy brain tissue of patients who were being treated for seizures. The patients had volunteered to help out in the experiment during lulls in their treatment, as electrodes had already been implanted over their auditory cortices to track the focal points of their seizures.

Researchers instructed the patients to perform such tasks as repeating words and vowels they heard, and recorded the activity. In comparing the activity of electrical signals discharged during speaking and hearing, they found that some regions of the auditory cortex showed less activity during speech, while others showed the same or higher levels.

"This shows that our brain has a complex sensitivity to our own speech that helps us distinguish between our vocalizations and those of others, and makes sure that what we say is actually what we meant to say," Flinker said.

Provided by University of California - Berkeley

Support a friend's work: Jia-Jen Lin.

2010-12-08T16:31:00.000-08:00

My practice investigates the psychological distance between artificial life and our physical sensations. By way of collecting, modifying, and representing information and materials from everyday experiences, I develop a series of works integrating sculpture, performance, and digital media.Mass-produced products and mechanical systems are manipulating our daily life and our physical sensations. We are not aware of the loss of intimate connections with our physical body, but we know we cannot live without technology.

Wearable structure and video performance as methods to investigate the potential visual dialogues between the body and the materials combined with the body. I would like to draw the attention to the initial stage: to investigate the possibilities between the material world and our physical selves.

In this work the crossing of the boundaries of media and categories becomes not only necessary, but natural. The readily available products of our society become my palette for representing the forms of the natural and for investigating relationships between people and between people and the technological

Think multitasking is new? Our prehistoric ancestors invented it

2010-12-08T07:42:00.000-08:00

Answering e-mail while toggling between telephone conversations. Monitoring social networking sites while working. Supervising the kids' homework while listening to the news and cooking dinner. The abundance of contemporary distractions offers many reasons to curse multitasking.

But a UCLA anthropologist refuses to join the chorus. In a new book that explores the long history of multitasking, Monica L. Smith maintains that human beings should appreciate their ability to sequence many activities and to remember to return to a task once it has been interrupted, possibly even with new ideas on how to improve the activity.

"I don't think it's worth saying multitasking is bad," said Smith, the author of "A Prehistory of Ordinary People" (University of Arizona Press). "We can do it, and that is astonishing."

In fact, Smith, an associate professor of anthropology, contends that the multitasking is the ability that separates human beings from animals: "Multitasking is what makes us human."

Vast reserves of memory and the ability to project into the future are the qualities that enable humans to juggle multiple competing demands and to pick up and put down the same project until completion, she said. Animals, by contrast, lack these abilities.

The same cognitive capacity enables such uniquely human abilities as language and the ability to comprehend time and space across increments ranging from the most immediate to the most distant, she contends. Smith also credits multitasking with our ancestor's considerable track record in innovation, particularly at the hands of ordinary people.

"Great deeds have been made possible by the collective experience of people who multitasked through their everyday lives ... and then who devoted some extra portion of their time, energy and the fruits of their labor into coming up with fabulous inventions and building complex societies," she said.

Yet in the popular imagination, contemporary times have some kind of corner on the multitasking market.

"People seem to think that the past was this simpler time with fewer interruptions because so many of the modern gadgets we have today had yet to be invented," Smith said. "But we've been multitasking from the beginning. Every object that we have from the past is the result of a dynamic process where people were being interrupted all the time."

Smith, who specializes in prehistoric economic networks and in the archaeology of consumption and material culture, traces the beginning of multitasking back millions of years to our first bipedal ancestors.

"Once they started walking on two feet, their hands were free to pick up tools, fibers, fruits or kids, and their eyes could look around for opportunities and dangers," she said. "That's the beginning of multitasking right there."

By the time tool-making started 1.5 million years ago, the ability to multitask would have been essential because the linear sequence of tool production would have been subject to frequent interruptions, she said.

For these hunters and gatherers, multitasking would have taken the form of foraging for food or hunting for game while keeping an eye out for stones and other materials with which to make tools, Smith said. Because children often would have been in tow, protecting them — especially from potential predators — would have been part of the mix.

Climate changes that made the globe drier and hotter some 10,000 to 12,000 years ago made the ability to multitask all the more valuable by paving the way for agriculture and animal husbandry, Smith said. Cycles of plant and animal life posed constant scheduling challenges and interruptions for these early settlers. Farm life also demanded the creation and maintenance of a whole new array of objects and structures for food storage, further increasing the need to juggle multiple tasks and priorities.

When humans first moved into cities about 6,000 years ago, the demands met by multitasking increased once again to levels that do not differ that much from today's levels, Smith insists.

"People were trying to cook things in the household while other people were trying to make things," she said. "Night would be coming along and tasks had to be finished before it got dark outside. The seasons would be changing, adding another layer of time pressure. Unexpected visitors would arrive and they'd need to be fed. Or someone was successful at hunting, so all of a sudden, a new animal would show up and everything has to be dropped so that the animal can get gutted, skinned, cleaned, chopped and stuck into stew pot."

Smith finds support for her theory by combining research from two fields. From archaeology, she takes the calculations extracted from archaeological digs to determine the number of people who occupied prehistoric sites and the kinds of human activities that were undertaken there — such as making tools, pots and beads. From anthropological studies of traditional people today, she takes estimates of how long it takes to make similar objects using similar approaches.

"We can calculate how much prehistoric people needed to eat, how long it takes to do a particular kind of task, and any seasonal restrictions on different tasks," Smith said. "We find that there's no way that you could sit down and do any of these things from start to finish. Multitasking had to be involved."

Multitasking also makes sense from a biological perspective, Smith argues, citing recent research by economists, folklorists, neurologists and archaeologists. Researchers have noted that the type of cognitive shortcuts involved in multitasking extends the number of activities humans can accomplish without having to tap higher-order cognitive abilities such as reasoning.

"Reasoning is expensive in time and energy, and the brain circuitry of multitasking reserves this 'expensive' ability for activities with the highest payoff, including decisions about cooperation or conflict with others and the subtleties of choosing among different types of goods and priorities," Brian Loasby, a professor emeritus of economics at Scotland's Stirling University, says in the book.

In addition to being efficient, the dynamic process of repeatedly putting down and picking up tasks by generation after generation of ordinary people has provided an important opportunity for innovation, Smith argues.

"Our ancestors might have set down the stone tool they were making for an hour, a day or a year because a new kid was born or somebody died or a flood came or dinner had to be made," she explained. "When they came back to the tool, they were not exactly the same people who had put it down. Maybe they had learned a new technique, gotten some new information about creating such an object or had thoughts about improving it by changing its shape."

By appreciating the role of multitasking, the role of ordinary people in laying the foundation for great civilizations comes into clearer focus, she argues.

"Every human-made object is the result of people who were consciously integrating all the things that they knew and were learning into the production process, speeding innovation," she said. "When leaders finally came into the picture and began organizing people to build tombs and temples, it was just another layer of activity on top of what ordinary people had already been doing for thousands of years."

Provided by University of California Los Angeles

QuantumDream, Inc. has just launched DNA Decipher Journal ("DNADJ") with Inaugural Issue in January 2011.

2010-12-07T20:08:00.000-08:00

DNA Decipher Journal is a publication in which biologists, physicists, mathematicians and other learned scholars publish their research results and express their views on the origin, nature and mechanism of DNA as a biological program and entity and its possible connection to a deeper reality. The journal is published by QuantumDream, Inc. We are committed to truth and excellence. The current policy at this journal is editorial selections of submitted papers for publication and editorial invitation for publication under the advisement of an editorial Advisory Board, members of which are under selections. All papers published by this journal are either subject to open-peer-review ("OPR") in the same issue or open to OPR in subsequent issues.

New study suggests that a propensity for one-night stands, uncommitted sex could be genetic

2010-12-02T10:24:00.000-08:00

New study suggests that a propensity for one-night stands, uncommitted sex could be genetic
December 1st, 2010 in Medicine & Health / Psychology & Psychiatry

So, he or she has cheated on you for the umpteenth time and their only excuse is: "I just can't help it." According to researchers at Binghamton University, they may be right. The propensity for infidelity could very well be in their DNA.

In a first of its kind study, a team of investigators led by Justin Garcia, a SUNY Doctoral Diversity Fellow in the laboratory of evolutionary anthropology and health at Binghamton University, State University of New York, has taken a broad look at sexual behavior, matching choices with genes and has come up with a new theory on what makes humans 'tick' when it comes to sexual activity. The biggest culprit seems to be the dopamine receptor D4 polymorphism, or DRD4 gene. Already linked to sensation-seeking behavior such as alcohol use and gambling, DRD4 is known to influence the brain's chemistry and subsequently, an individual's behavior.

"We already know that while many people experience sexual activity, the circumstances, meaning and behavior is different for each person," said Garcia. "Some will experience sex with committed romantic partners, others in uncommitted one-night stands. Many will experience multiple types of sexual relationships, some even occurring at the same time, while others will exchange sex for resources or money. What we didn't know was how we are motivated to engage in one form and not another, particularly when it comes to promiscuity and infidelity."

Gathering a detailed history of the sexual behavior and intimate relationships of 181 young adults along with samples of their DNA, Garcia and his team of investigators were able to determine that individual differences in sexual behavior could indeed be influenced by individual genetic variation.

"What we found was that individuals with a certain variant of the DRD4 gene were more likely to have a history of uncommitted sex, including one-night stands and acts of infidelity," said Garcia. "The motivation seems to stem from a system of pleasure and reward, which is where the release of dopamine comes in. In cases of uncommitted sex, the risks are high, the rewards substantial and the motivation variable – all elements that ensure a dopamine 'rush.'"

According to Garcia, these results provide some of the first biological evidence that at first glance, seems to be somewhat of a contradiction: that individuals could be looking for a serious committed long-term relationship, but have a history of one-night stands. At the same time, the data also suggests it is also reasonable that someone could be wildly in love with their partner, commit infidelity, and yet still be deeply attached and care for their partner. It all came back to a DRD4 variation in these individuals. Individual differences in the internal drive for a dopamine 'rush' can function independently from the drive for commitment.

"The study doesn't let transgressors off the hook," said Garcia. "These relationships are associative, which means that not everyone with this genotype will have one-night stands or commit infidelity. Indeed, many people without this genotype still have one-night stands and commit infidelity. The study merely suggests that a much higher proportion of those with this genetic type are likely to engage in these behaviors."

Garcia also cautions that the consequences of risky sexual behavior can indeed be extreme.

"One-night stands can be risky, both physically and psychologically," said Garcia. "And betrayal can be one of the most devastating things to happen to a couple. These genes do not give anyone an excuse, but they do provide a window into how our biology shapes our propensities for a wide variety of behaviors."

At this point, very little is known about how genetics and neurobiology influence one's sexuality propensities and tendencies but Garcia is hopeful that this study will add to the growing base of knowledge - in particular, how genes might predispose individuals to pursue sensation seeking across all sorts of domains – from substance use to sexuality. This study also provides further support for the notion that the biological foundations for sexual desire may often operate independently from, although absolutely linked to, deep feelings of romantic attachment.

As Garcia points out, he and his team of study co-authors have only just begun to explore the issue and plan on conducting a series of follow-up and related studies.

"We want to run a larger sample of men and women to replicate these findings and check for several other possible genetic markers," said Garcia.

"We will also be conducting a number of behavioral and biological studies to better understand what kinds of associated factors motivate uncommitted sexual behavior. Most importantly, we want to explore the receiving end of infidelity by looking at how people respond to cases of uncommitted sex and infidelity."

More information: A detailed report can be found in the current issue of Public Library of Science's PLoS ONE journal. The article, "Associations between Dopamine D4 Receptor Gene Variation with Both Infidelity and Sexual Promiscuity," can be found at http://dx.plos.org … pone.0014162

Provided by Binghamton University