Researchers Confirm Multiple Genes Robustly Contribute to Schizophrenia Risk in Replication

Multiple genes contribute to risk for schizophrenia and appear to function in pathways related to transmission of signals in the brain and immunity, according to an international study led by Virginia Commonwealth University School of Pharmacy researchers.

By better understanding the molecular and biological mechanisms involved with schizophrenia, scientists hope to use this new genetic information to one day develop and design drugs that are more efficacious and have fewer side effects.

In a study published online in the April issue of JAMA Psychiatry, the JAMA Network journal, researchers used a comprehensive and unique approach to robustly identify genes and biological processes conferring risk for schizophrenia.

The researchers first used 21,953 subjects to examine over a million genetic markers. They then systematically collected results from other kinds of biological schizophrenia studies and combined all these results using a novel data integration approach.

The most promising genetic markers were tested again in a large collection of families with schizophrenia patients, a design that avoids pitfalls that have plagued genetic studies of schizophrenia in the past. The genes they identified after this comprehensive approach were found to have involvement in brain function, nerve cell development and immune response.

“Now that we have genes that are robustly associated with schizophrenia, we can begin to design much more specific experiments to understand how disruption of these genes may affect brain development and function,” said principal investigator Edwin van den Oord, Ph.D., professor and director of the Center for Biomarker Research and Personalized Medicine in the Department of Pharmacotherapy and Outcomes Science at the VCU School of Pharmacy.

“Also, some of these genes provide excellent targets for the development of new drugs,” he said.

One specific laboratory experiment currently underway at VCU to better understand the function of one of these genes, TCF4, is being led by Joseph McClay, Ph.D., a co-author on the study and assistant professor and laboratory director in the VCU Center for Biomarker Research and Personalized Medicine. TCF4 works by switching on other genes in the brain. McClay and colleagues are conducting a National Institutes of Health-funded study to determine all genes that are under the control of TCF4. By mapping the entire network, they aim to better understand how disruptions to TCF4 increase risk for schizophrenia.

“Our results also suggest that the novel data integration approach used in this study is a promising tool that potentially can be of great value in studies of a large variety of complex genetic disorders,” said lead author Karolina A. Aberg, Ph.D., research assistant professor and laboratory co-director of the Center for Biomarker Research and Personalized Medicine in the VCU School of Pharmacy.

(Image: iStockphoto)

Awake imaging device moves diagnostics field forward

A technology being developed at the Department of Energy’s Oak Ridge National Laboratory promises to provide clear images of the brains of children, the elderly and people with Parkinson’s and other diseases without the use of uncomfortable or intrusive restraints.

Awake imaging provides motion compensation reconstruction, which removes blur caused by motion, allowing physicians to get a transparent picture of the functioning brain without anesthetics that can mask conditions and alter test results. The use of anesthetics, patient restraints or both is not ideal because they can trigger brain activities that may alter the normal brain functions being studied.

With this new capability, researchers hope to better understand brain development in babies, pre-teens and teen-agers. In addition, they believe the technology will provide unprecedented insight into conditions such as autism, drug addictions, alcoholism, traumatic brain injuries and Alzheimer’s disease.

"With this work, we’re hoping to establish a new paradigm in noninvasive diagnostic imaging," said Justin Baba, a biomedical engineer who heads the ORNL development team.

The study, which was performed in collaboration with Thomas Jefferson National Accelerator Laboratory and Johns Hopkins University, utilized an awake imaging scanner and awake, unanesthetized, unrestrained mice that had been injected with a radiotracer known as DaTSCAN, provided by GE-Medical.

With awake imaging using DaTSCAN and other molecular probes, Baba and colleagues envision development of new, more effective therapies for a wide assortment of conditions and diseases while also contributing to pharmaceutical drug discovery, development and testing. The technology could also help with real-time stabilization and registration of targets during surgical intervention.

Baba noted that this technical accomplishment, detailed in a paper published in The Journal of Nuclear Medicine, has its origins in past DOE-supported research on biomedical imaging. The paper is titled “Conscious, Unrestrained Molecular Imaging of Mice with AwakeSPECT.” Jim Goddard of ORNL’s Measurement Science and Systems Engineering Division is a co-author.

While a working prototype scanner is located at Johns Hopkins School of Medicine, ORNL is pursuing commercialization of the technology.

Pesticide combination affects bees’ ability to learn

Two new studies have highlighted a negative impact on bees’ ability to learn following exposure to a combination of pesticides commonly used in agriculture. The researchers found that the pesticides, used in the research at levels shown to occur in the wild, could interfere with the learning circuits in the bee’s brain. They also found that bees exposed to combined pesticides were slower to learn or completely forgot important associations between floral scent and food rewards.

In the study published today (27 March 2013) in Nature Communications, the University of Dundee’s Dr Christopher Connolly and his team investigated the impact on bees’ brains of two common pesticides: pesticides used on crops called neonicotinoid pesticides, and another type of pesticide, coumaphos, that is used in honeybee hives to kill the Varroa mite, a parasitic mite that attacks the honey bee.

The intact bees’ brains were exposed to pesticides in the lab at levels predicted to occur following exposure in the wild and brain activity was recorded. They found that both types of pesticide target the same area of the bee brain involved in learning, causing a loss of function. If both pesticides were used in combination, the effect was greater.

The study is the first to show that these pesticides have a direct impact on pollinator brain physiology. It was prompted by the work of collaborators Dr Geraldine Wright and Dr Sally Williamson at Newcastle University who found that combinations of these same pesticides affected learning and memory in bees. Their studies established that when bees had been exposed to combinations of these pesticides for 4 days, as many as 30% of honeybees failed to learn or performed poorly in memory tests. Again, the experiments mimicked levels that could be seen in the wild, this time by feeding a sugar solution mixed with appropriate levels of pesticides.

Dr Geraldine Wright said: “Pollinators perform sophisticated behaviours while foraging that require them to learn and remember floral traits associated with food. Disruption in this important function has profound implications for honeybee colony survival, because bees that cannot learn will not be able to find food.”

Together the researchers expressed concerns about the use of pesticides that target the same area of the brain of insects and the potential risk of toxicity to non-target insects. Moreover, they said that exposure to different combinations of pesticides that act at this site may increase this risk.

Dr Christopher Connolly said: “Much discussion of the risks posed by the neonicotinoid insecticides has raised important questions of their suitability for use in our environment. However, little consideration has been given to the miticidal pesticides introduced directly into honeybee hives to protect the bees from the Varroa mite. We find that both have negative impact on honeybee brain function.

"Together, these studies highlight potential dangers to pollinators of continued exposure to pesticides that target the insect nervous system and the importance of identifying combinations of pesticides that could profoundly impact pollinator survival."

Researchers discover the brain origins of variation in pathological anxiety

New findings from nonhuman primates suggest that an overactive core circuit in the brain, and its interaction with other specialized circuits, accounts for the variability in symptoms shown by patients with severe anxiety. In a brain-imaging study published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the University of Wisconsin School of Medicine and Public Health describe work that for the first time provides an understanding of the root causes of clinical variability in anxiety disorders.

Using a well-established nonhuman primate model of childhood anxiety, the scientists identified a core circuit that is chronically over-active in all anxious individuals, regardless of their particular pattern of symptoms. They also identified a set of more specialized circuits that are over- or under-active in individuals prone to particular symptoms, such as chronically high levels of the stress-hormone cortisol.

“These findings provide important new insights into altered brain functioning that explains why people with anxiety have such different symptoms and clinical presentations, and it also gives us new ideas, based on an understanding of altered brain function, for helping people with different types of anxiety,’’ says Ned Kalin, senior author, chair of Psychiatry and director of the HealthEmotions Research Institute.

“There is a large need for new treatment strategies, because our current treatments don’t work well for many anxious adults and children who come to us for help.”

In the study, key anxiety-related symptoms were measured in 238 young rhesus monkeys using behavioral and hormonal measurement procedures similar to those routinely used to assess extreme shyness in children. Young monkeys are ideally suited for these studies because of their similarities in brain development and social behavior, Kalin notes. Variation in brain activity was quantified in the monkeys using positron emission tomography (PET) imaging, a method that is also used in humans.

Combining behavioral measures of shyness, physiological measures of the stress-hormone cortisol, and brain metabolic imaging, co-lead authors Alexander Shackman, Andrew Fox and their collaborators showed that a core neural system marked by elevated activity in the central nucleus of the amygdala was a consistent brain signature shared by young monkeys with chronically high levels of anxiety. This was true despite striking differences across monkeys in the predominance of particular anxiety-related symptoms.

The Wisconsin researchers also showed that young monkeys with particular anxiety profiles, such as high levels of shyness, showed changes in symptom-specific brain circuits. Finally, Shackman, Fox and colleagues uncovered evidence that the two kinds of brain circuits, one shared by all anxious individuals, the other specific to those with particular symptoms, work together to produce different presentations of pathological anxiety.

The new study builds upon earlier work by the Kalin laboratory demonstrating that activity in the amygdala is strongly shaped by early-life experiences, such as parenting and social interactions. They hypothesize that extreme anxiety stems from problems with the normal maturation of brain systems involved in emotional learning, which suggests that anxious children have difficulty learning to effectively regulate brain anxiety circuits. Taken together, this line of research sets the stage for improved strategies for preventing extreme childhood anxiety from blossoming into full-blown anxiety disorders.

“This means the amygdala is an extremely attractive target for new, broad-spectrum anxiety treatments,’’ says Shackman. “The central nucleus of the amygdala is a uniquely malleable substrate for anxiety, one that can help to trigger a wide range of symptoms.”

The work also suggests more specific brain targets for different symptom profiles. Such therapies could range from new, more selectively targeted medications to intensive therapies that seek to re-train the amygdala, ranging from conventional cognitive-behavioral therapies to training in mindfulness and other techniques, Shackman noted. To further understand the clinical significance of these observations, the laboratory is conducting a parallel study in young children suffering from anxiety disorders.

Unraveling the molecular roots of Down syndrome

Researchers discover that the extra chromosome inherited in Down syndrome impairs learning and memory because it leads to low levels of SNX27 protein in the brain.

What is it about the extra chromosome inherited in Down syndrome—chromosome 21—that alters brain and body development? Researchers have new evidence that points to a protein called sorting nexin 27, or SNX27. SNX27 production is inhibited by a molecule encoded on chromosome 21. The study, published March 24 in Nature Medicine, shows that SNX27 is reduced in human Down syndrome brains. The extra copy of chromosome 21 means a person with Down syndrome produces less SNX27 protein, which in turn disrupts brain function. What’s more, the researchers showed that restoring SNX27 in Down syndrome mice improves cognitive function and behavior.

“In the brain, SNX27 keeps certain receptors on the cell surface—receptors that are necessary for neurons to fire properly,” said Huaxi Xu, Ph.D., Sanford-Burnham professor and senior author of the study. “So, in Down syndrome, we believe lack of SNX27 is at least partly to blame for developmental and cognitive defects.”

SNX27’s role in brain function

Xu and colleagues started out working with mice that lack one copy of the snx27 gene. They noticed that the mice were mostly normal, but showed some significant defects in learning and memory. So the team dug deeper to determine why SNX27 would have that effect. They found that SNX27 helps keep glutamate receptors on the cell surface in neurons. Neurons need glutamate receptors in order to function correctly. With less SNX27, these mice had fewer active glutamate receptors and thus impaired learning and memory.

SNX27 levels are low in Down syndrome

Then the team got thinking about Down syndrome. The SNX27-deficient mice shared some characteristics with Down syndrome, so they took a look at human brains with the condition. This confirmed the clinical significance of their laboratory findings—humans with Down syndrome have significantly lower levels of SNX27.

Next, Xu and colleagues wondered how Down syndrome and low SNX27 are connected—could the extra chromosome 21 encode something that affects SNX27 levels? They suspected microRNAs, small pieces of genetic material that don’t code for protein, but instead influence the production of other genes. It turns out that chromosome 21 encodes one particular microRNA called miR-155. In human Down syndrome brains, the increase in miR-155 levels correlates almost perfectly with the decrease in SNX27.

Xu and his team concluded that, due to the extra chromosome 21 copy, the brains of people with Down syndrome produce extra miR-155, which by indirect means decreases SNX27 levels, in turn decreasing surface glutamate receptors. Through this mechanism, learning, memory, and behavior are impaired.

Restoring SNX27 function rescues Down syndrome mice

If people with Down syndrome simply have too much miR-155 or not enough SNX27, could that be fixed? The team explored this possibility. They used a noninfectious virus as a delivery vehicle to introduce new human SNX27 in the brains of Down syndrome mice.

“Everything goes back to normal after SNX27 treatment. It’s amazing—first we see the glutamate receptors come back, then memory deficit is repaired in our Down syndrome mice,” said Xin Wang, a graduate student in Xu’s lab and first author of the study. “Gene therapy of this sort hasn’t really panned out in humans, however. So we’re now screening small molecules to look for some that might increase SNX27 production or function in the brain.”

DNA damage occurs as part of normal brain activity

Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer’s disease—and identified two therapeutic strategies that reduce these disruptions.

Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer’s. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learning—as long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brain—widely thought to be a major cause of Alzheimer’s disease—increases the number of neurons with DSBs and delays their repair.

"It is both novel and intriguing team’s finding that the accumulation and repair of DSBs may be part of normal learning," said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. "Their discovery that the Alzheimer’s-like mice exhibited higher baseline DSBs, which weren’t repaired, increases these findings’ relevance and provides new understanding of this deadly disease’s underlying mechanisms."

In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer’s, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.

The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environment—but after being returned to their home environment, DSB levels dropped.

"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper’s lead author. "But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."

The group of mice modified to simulate Alzheimer’s had higher DSB levels at the start—levels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.

To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studies—one of which was led by Dr. Mucke and his team—that showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer’s and in humans in the disease’s earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tau—another protein implicated in Alzheimer’s. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.

The team’s findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer’s—perhaps by maintaining the delicate balance between DNA damage and repair.

"Currently, we have no effective treatments to slow, prevent or halt Alzheimer’s, from which more than 5 million people suffer in the United States alone," said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. "The need to decipher the causes of Alzheimer’s and to find better therapeutic solutions has never been more important—or urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memory—and in the disruption of these important brain functions by Alzheimer’s disease."

(Image courtesy: Lulu Qian, Erik Winfree & Jehoshua Bruck | California Institute of Technology)

The neuroscience of finding your lost keys

Ever find yourself racking your brain on a Monday morning to remember where you put your car keys?

When you do find those keys, you can thank the hippocampus, a brain region responsible for storing and retrieving memories of different environments-such as that room where your keys were hiding in an unusual spot.

Now, scientists have helped explain how the brain keeps track of the incredibly rich and complex environments people navigate on a daily basis. They discovered how the dentate gyrus, a subregion of the hippocampus, helps keep memories of similar events and environments separate, a finding they reported March 20 in eLife. The findings, which clarify how the brain stores and distinguishes between memories, may also help identify how neurodegenerative diseases, such as Alzheimer’s disease, rob people of these abilities.

"Everyday, we have to remember subtle differences between how things are today, versus how they were yesterday - from where we parked our car to where we left our cellphone," says Fred H. Gage, senior author on the paper and the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease at Salk. "We found how the brain makes these distinctions, by storing separate ‘recordings’ of each environment in the dentate gyrus."

The process of taking complex memories and converting them into representations that are less easily confused is known as pattern separation. Computational models of brain function suggest that the dentate gyrus helps us perform pattern separation of memories by activating different groups of neurons when an animal is in different environments.

However, previous laboratory studies found that in fact the same populations of neurons in the dentate gyrus are active in different environments, and that the way the cells distinguished new surroundings was by changing the rate at which they sent electrical impulses. This discrepancy between theoretical predictions and laboratory findings has perplexed neuroscientists and obscured our understanding of memory formation and retrieval.

To explore this mystery more deeply, the Salk scientists compared the functioning of the mouse dentate gyrus and another region of the hippocampus, known as CA1, using laboratory techniques for tracking the activity of neurons at multiple time points.

First, the researchers took mice from their original chamber and placed them in a novel chamber to learn about a new environment (episode 1). Meanwhile, they recorded which hippocampal neurons were active as the animals responded to their new surroundings. Subsequently, the mice were either returned to that same novel chamber to measure memory recall or to a slightly modified chamber to measure discrimination (episode 2). The active neurons in episode 2 were also labeled in order to determine if the neurons activated in episode 1 were used in the same way for recall and for discrimination of small differences between environments.

When the researchers compared the neural activity during the two episodes, they found that the dentate gyrus and CA1 sub-regions functioned differently. In CA1, the same neurons that were active during the initial learning episode were also active when the mice retrieved the memories. In the dentate gyrus, however, distinct groups of cells were active during the learning episodes and retrieval. Also, exposing the mice to two subtly different environments activated two distinct groups of cells in the dentate gyrus.

"This finding supported the predictions of theoretical models that different groups of cells are activated during exposure to similar, but distinct, environments," says Wei Deng, a Salk postdoctoral research and first author on the paper. "This contrasts with the findings of previous laboratory studies, possibly because they looked at different sub-populations of neurons in the dentate gyrus."

The Salk researchers’ findings suggest that recalling a memory-such as the location of missing keys-does not always involve reactivation of the same neurons that were active during encoding. More importantly, the results indicate that the dentate gyrus performs pattern separation by using distinct populations of cells to represent similar but non-identical memories.

The findings help clarify the mechanisms that underpin memory formation and shed light on systems that are disrupted by injuries and diseases of the nervous system.

Researchers image most of vertebrae brain at single cell level

Misha Ahrens and Philipp Keller, researchers with the Howard Hughes Medical Institute have succeeded in making a near real-time video of most of a zebrafish’s brain showing individual neuron cells firing. To create the video, as the team reports in their paper published in the journal Nature Methods, the two developed a type of modified light-sheet microscopy and used it in on genetically modified fish.

To create the video, the researchers turned to zebrafish in their larval state—their brains are transparent and small. To cause firing neurons to be visible they genetically altered the fish’s brains, giving them a protein that glows when responding to changes in calcium ion levels, which happen when nerve cells fire. Next, they used a microscope that was able to broadcast a sheet of light through the fish’s brain allowing for the detection of the firing neurons. The system recorded images every 1.3 seconds. The final step was stitching the images together to create a video. The result is nothing short of breathtaking—looking like something out of a science fiction movie’s special effects department.

The video marks the first visual capture of most of a living vertebrae brain at the neuron level, as it works in near real-time and offers striking evidence of the complexity of the brain—even one as small as 100,000 neurons. The researchers say their video shows approximately 80 percent of the zebrafish’s brain as it operates—though what all those firing neurons represent in particular, is still unknown.

The researchers are careful to point out that what they’ve accomplished does not portend the creation of a video of a human brain in action—our brains are much larger, have billions more neurons and perhaps more importantly, are not transparent and are covered by a thick skull. Instead they suggest that studying a simpler brain in action might help to explain how biological neural networks actually work, perhaps leading to theories that can be generalized over larger animals.

But before that can happen, the procedure the team has developed needs to be improved—neurons can fire at hundreds of times per second, which means a lot of firing in the video has been missed. Capturing at a faster rate would mean generating nearly unmanageable amounts of data—at the current rate, just one hour of capture creates a terabyte of data. Thus a new way to store and process the data must be developed.

Neuro-magic: Magician uses magic tricks to study the brain’s powers of perception and memory

A magician is using his knowledge of magic theory and practice to investigate the brain’s powers of observation.

Hugo Caffaratti, engineer and semi-professional magician from Barcelona, Spain, has embarked on a PhD with the University of Leicester’s Centre for Systems Neuroscience.

Hugo has 12 years of experience working with magic – specialising in card tricks – and is a member of the Spanish Society of Illusionism (SEI-ACAI).

The engineer also has a longstanding interest in neuroscience and bioengineering, having taken a Master’s degree in Biomedical Engineering at University of Barcelona.

He hopes to combine his two interests in his PhD thesis project, which covers a new field of Cognitive Neuroscience: Neuro-Magic.

As part of his work, he will investigate how our brains perceive what actually happens before our eyes – and how our attention can be drawn away from important details.

He also plans to study “forced choice” - a tool often used by magicians where we are fooled into thinking we have made a free choice.

Among other experiments, Hugo will ask participants to watch videos of card trick performances, while sitting in front of an eye-tracker device.

This will allow him to monitor where our attention is focused during illusions – and how our brain can be deceived when our eyes miss the whole picture.

Hugo said: “I have always been interested in the study of the brain. It is amazing to be involved in the process of combining the disciplines of neuroscience and magic.

“I am really interested in the fields of decision making and forced-choice. It is incredible that many times a day we make a decision and feel free. We do not realise that we have been forced to make that decision.

“I am constructing an experiment to study what happens when we make forced decisions – to try and find the reasons for it. I am thinking about which kinds of tricks I know could be useful to give more insights about brain function.”

He will work under the tutelage of Professor Rodrigo Quian Quiroga, director of the Centre for Systems Neuroscience.

Professor Quian Quiroga’s recent work on memory formation was the topic of his recent book “Borges and memory” (MIT Press) and was also featured on the front page of the international science publication Scientific American.

Professor Rodrigo Quian Quiroga said: “I am very interested in connections between science and the arts. Last year, for example, we organized an art and science exhibition as a result of a 1-year rotation in my lab of visual artist Mariano Molina. Hugo’s PhD will look at decision-making and attention – and although he is doing his first steps in neuroscience, I think he already has a lot of expertise in this area based on his training as a magician.

“Magic theory has thousands of years of experience. Magicians have been answering similar questions that we have in the lab, and they have an intuitive knowledge of how the mind works. Hugo will likely bring a fresh new view on how to address questions we deal with in neuroscience.”

Hugo is also keen to carry on with his work in magic while studying for his PhD, and is hoping to perform in bars in Leicester while staying here.

He has also applied for membership with The Magic Circle – a prestigious magic society of London. He will have to sit exams to prove his magical mettle in order to join the exclusive club.

One region, two functions: Brain cells’ multitasking may be a key to understanding overall brain function

A region of the brain known to play a key role in visual and spatial processing has a parallel function: sorting visual information into categories, according to a new study by researchers at the University of Chicago.

Primates are known to have a remarkable ability to place visual stimuli into familiar and meaningful categories, such as fruit or vegetables. They can also direct their spatial attention to different locations in a scene and make spatially-targeted movements, such as reaching.

The study, published in the March issue of Neuron, shows that these very different types of information can be simultaneously encoded within the posterior parietal cortex. The research brings scientists a step closer to understanding how the brain interprets visual stimuli and solves complex tasks.

“We found that multiple functions can be mapped onto a particular region of the brain and even onto individual brain cells in that region,” said study author David Freedman, PhD, assistant professor of neurobiology at the University of Chicago. “These functions overlap. This particular brain area, even its individual neurons, can independently encode both spatial and cognitive signals.”

Freedman studies the effects of learning on the brain and how information is stored in short-term memory, with a focus on the areas that process visual stimuli. To examine this phenomenon, he has taught monkeys to play a simple video game in which they learn to assign moving visual patterns into categories.

“The task is a bit like a baseball umpire calling balls and strikes,” he said, “since the monkeys have to sort the various motion patterns into two groups, or categories.”

The monkeys master the tasks over a few weeks of training. Once they do, the researchers record electrical signals from parietal lobe neurons while the subjects perform the categorization task. By measuring electrical activity patterns of these neurons, the researchers can decode the information conveyed by the neurons’ activity.

“The activity patterns in these parietal neurons carry strong information about the category that each motion pattern gets assigned to during the task,” Freedman said.

(Image: Thinkstock)