jueves, 31 de marzo de 2011
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.
viernes, 25 de marzo de 2011
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
viernes, 18 de marzo de 2011
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
jueves, 10 de marzo de 2011
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
martes, 1 de marzo de 2011
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