August 13, 2014

New Study Points to a Brain Region Key to Contextual Memories

Dartmouth researchers demonstrate in a new study that a previously understudied part of the brain, the retrosplenial cortex, is essential for forming the basis for contextual memories, which help you to recall events ranging from global disasters to where you parked your car.

An important aspect of memory is the ability to recall the physical place, or context, in which an event occurred. For example, in recalling emotionally charged events such as the September 11 terror attacks or the assassination of President John F. Kennedy, we remember not only the event but also where we were when it happened. Indeed, in discussing such events with others, we often ask, “Where were you when … ?” Processing “where” information is also important for mundane events such as remembering where you parked your car.

Although it is known that a specific network of brain regions is important for contextual memory, it has not been known how different parts of the network contribute to this process. But using a newly developed technology known as “chemogenetics,” Professor David Bucci’s laboratory is beginning to show how different brain structures contribute to contextual learning and memory. Developed at the University of North Carolina School of Medicine, the chemogenetics technique enables researchers to “remotely control” the activity of brains cells. This is accomplished by using a virus to transfers genes for a synthetic receptor into a brain region. The receptors are responsive only to a synthetic drug that is administered through a simple injection. By binding to the receptors, the drug temporarily turns off—or on—brain cells in that region for a short amount of time.

Using this approach, Bucci’s laboratory demonstrated in an experiment with rats that the retrosplenial cortex is critical for forming the basis for contextual memories. It was the first time the chemogenetics technique had been used to turn off cells along the entire retrosplenial cortex. The importance of this finding is underscored by two recent studies showing that the hippocampus, another key brain region involved in contextual memories, is not itself active or necessary for forming the initial associations that underlie contextual memory.

The National Science Foundation recently awarded Bucci a five-year, $725,000 grant to continue this research.

“By providing new insight into the function of this part of the brain, our work will also have implications for understanding the basis for illnesses that impact contextual memory, such as Alzheimer’s disease,” Bucci says. “In fact, recent studies have shown that the retrosplenial cortex is one of the first brain areas that is damaged in persons with Alzheimer’s disease.”

The findings appear in The Journal of Neuroscience.

(Source: now.dartmouth.edu)

Filed under retrosplenial cortex contextual memory memory brain cells chemogenetics neuroscience science

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August 13, 2014

Treating Mental Illness by Changing Memories of Things Past

In the novel À larecherche du temps perdu (translated into English as Remembrance of Things Past), Marcel Proust makes a compelling case that our identities and decisions are shaped in profound and ongoing ways by our memories.

This truth is powerfully reflected in mental illnesses,like post traumatic stress disorder (PTSD) and addictions. In PTSD, memories of traumas intrude vividly upon consciousness, causing distress, driving people to avoid reminders of their traumas, and increasing risk for addiction and suicide. In addiction, memories of drug use influence reactions to drug-related cues and motivate compulsive drug use.

What if one could change these dysfunctional memories? Although we all like to believe that our memories are reliable and permanent, it turns out that memories may indeed be plastic.

The process for modifying memories, depicted in the graphic, is called memory reconsolidation. After memories are formed and stored, subsequent retrieval may make them unstable. In other words, when a memory is activated, it also becomes open to revision and reconsolidation in a new form.

"Memory reconsolidation is probably among the most exciting phenomena in cognitive neuroscience today. It assumes that memories may be modified once they are retrieved which may give us the great opportunity to change seemingly robust, unwanted memories," explains Dr. Lars Schwabe of Ruhr-University Bochum in Germany. He and his colleagues have authored a review paper on the topic, published in the current issue of Biological Psychiatry.

The idea of memory reconsolidation was initially discovered and demonstrated in rodents.

The first evidence of reconsolidation in humans was reported in a study in 2003, and the findings have since continued to accumulate. The current report summarizes the most recent findings on memory reconsolidation in humans and poses additional questions that must be answered by future studies.

"Reconsolidation appears to be a fundamental process underlying cognitive and behavioral therapies. Identifying its roles and mechanisms is an important step forward to fully harnessing the reconsolidation process in psychotherapy," said Dr. John Krystal, Editor of Biological Psychiatry.

The translation of the animal data to humans is a vital step for the potential application of memory reconsolidation in the context of mental disorders. Memory reconsolidation could open the door to novel treatment approaches for disorders such as PTSD or drug addiction.

Filed under hippocampus memory memory reconsolidation PTSD drug addiction neuroscience science

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August 13, 2014

A Gene Linked to Disease Found to Play a Critical Role in Normal Memory Development

It has been more than 20 years since scientists discovered that mutations in the gene huntingtin cause the devastating progressive neurological condition Huntington’s disease, which involves involuntary movements, emotional disturbance and cognitive impairment. Surprisingly little, however, has been known about the gene’s role in normal brain activity.

Now, a study from The Scripps Research Institute’s (TSRI’s) Florida campus and Columbia University shows it plays a critical role in long-term memory.

“We found that huntingtin expression levels are necessary for what is known as long-term synaptic plasticity—the ability of the synapses to grow and change—which is critical to the formation of long-term memory,” said TSRI Assistant Professor Sathyanarayanan V. Puthanveettil, who led the study with Nobel laureate Eric Kandel of Columbia University.

In the study, published recently by the journal PLOS ONE, the team identified an equivalent of the human huntingtin protein in the marine snail Aplysia, a widely used animal model in genetic studies, and found that, just like its human counterpart, the protein in Aplysia is widely expressed in neurons throughout the central nervous system.

Using cellular models, the scientists studied what is known as the sensory-to-motor neuron synapse of Aplysia—in this case, gill withdrawal, a defensive move that occurs when the animal is disturbed.

The study found that the expression of messenger RNAs of huntingtin—messenger RNAs are used to produce proteins from instructions coded in genes—is increased by serotonin, a neurotransmitter released during learning in Aplysia. After knocking down production of the huntingtin protein, neurons failed to function normally.

“During the learning, production of the huntingtin mRNAs is increased both in pre- and post-synaptic neurons—that is a new finding,” Puthanveettil said. “And if you block production of the protein either in pre- or post-synaptic neuron, you block formation of memory.”

The findings could have implications for the development of future treatments of Huntington’s disease. While the full biological functions of the huntingtin protein are not yet fully understood, the results caution against a therapeutic approach that attempts to eliminate the protein entirely.

Filed under huntington’s disease huntingtin aplysia memory formation synaptic plasticity neuroscience science

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August 13, 2014

Bioengineers Create Functional 3D Brain-like Tissue

Bioengineers have created three-dimensional brain-like tissue that functions like and has structural features similar to tissue in the rat brain and that can be kept alive in the lab for more than two months.

As a first demonstration of its potential, researchers used the brain-like tissue to study chemical and electrical changes that occur immediately following traumatic brain injury and, in a separate experiment, changes that occur in response to a drug. The tissue could provide a superior model for studying normal brain function as well as injury and disease, and could assist in the development of new treatments for brain dysfunction.

The brain-like tissue was developed at the Tissue Engineering Resource Center at Tufts University, Boston, which is funded by the National Institute of Biomedical Imaging and Bioengineering (NIBIB) to establish innovative biomaterials and tissue engineering models. David Kaplan, Ph.D., Stern Family Professor of Engineering at Tufts University is director of the center and led the research efforts to develop the tissue.

Currently, scientists grow neurons in petri dishes to study their behavior in a controllable environment. Yet neurons grown in two dimensions are unable to replicate the complex structural organization of brain tissue, which consists of segregated regions of grey and white matter. In the brain, grey matter is comprised primarily of neuron cell bodies, while white matter is made up of bundles of axons, which are the projections neurons send out to connect with one another. Because brain injuries and diseases often affect these areas differently, models are needed that exhibit grey and white matter compartmentalization.

Recently, tissue engineers have attempted to grow neurons in 3D gel environments, where they can freely establish connections in all directions. Yet these gel-based tissue models don’t live long and fail to yield robust, tissue-level function. This is because the extracellular environment is a complex matrix in which local signals establish different neighborhoods that encourage distinct cell growth and/or development and function. Simply providing the space for neurons to grow in three dimensions is not sufficient.

Now, in the Aug. 11th early online edition of the journal Proceedings of the National Academy of Sciences, a group of bioengineers report that they have successfully created functional 3D brain-like tissue that exhibits grey-white matter compartmentalization and can survive in the lab for more than two months.

“This work is an exceptional feat,” said Rosemarie Hunziker, Ph.D., program director of Tissue Engineering at NIBIB. “It combines a deep understand of brain physiology with a large and growing suite of bioengineering tools to create an environment that is both necessary and sufficient to mimic brain function.”

The key to generating the brain-like tissue was the creation of a novel composite structure that consisted of two biomaterials with different physical properties: a spongy scaffold made out of silk protein and a softer, collagen-based gel. The scaffold served as a structure onto which neurons could anchor themselves, and the gel encouraged axons to grow through it.

To achieve grey-white matter compartmentalization, the researchers cut the spongy scaffold into a donut shape and populated it with rat neurons. They then filled the middle of the donut with the collagen-based gel, which subsequently permeated the scaffold. In just a few days, the neurons formed functional networks around the pores of the scaffold, and sent longer axon projections through the center gel to connect with neurons on the opposite side of the donut. The result was a distinct white matter region (containing mostly cellular projections, the axons) formed in the center of the donut that was separate from the surrounding grey matter (where the cell bodies were concentrated).

Over a period of several weeks, the researchers conducted experiments to determine the health and function of the neurons growing in their 3D brain-like tissue and to compare them with neurons grown in a collagen gel-only environment or in a 2D dish. The researchers found that the neurons in the 3D brain-like tissues had higher expression of genes involved in neuron growth and function. In addition, the neurons grown in the 3D brain-like tissue maintained stable metabolic activity for up to five weeks, while the health of neurons grown in the gel-only environment began to deteriorate within 24 hours. In regard to function, neurons in the 3D brain-like tissue exhibited electrical activity and responsiveness that mimic signals seen in the intact brain, including a typical electrophysiological response pattern to a neurotoxin.

Because the 3D brain-like tissue displays physical properties similar to rodent brain tissue, the researchers sought to determine whether they could use it to study traumatic brain injury. To simulate a traumatic brain injury, a weight was dropped onto the brain-like tissue from varying heights. The researchers then recorded changes in the neurons’ electrical and chemical activity, which proved similar to what is ordinarily observed in animal studies of traumatic brain injury.

Kaplan says the ability to study traumatic injury in a tissue model offers advantages over animal studies, in which measurements are delayed while the brain is being dissected and prepared for experiments. “With the system we have, you can essentially track the tissue response to traumatic brain injury in real time,” said Kaplan. “Most importantly, you can also start to track repair and what happens over longer periods of time.”

Kaplan emphasized the importance of the brain-like tissue’s longevity for studying other brain disorders. “The fact that we can maintain this tissue for months in the lab means we can start to look at neurological diseases in ways that you can’t otherwise because you need long timeframes to study some of the key brain diseases,” he said.

Hunziker added, “Good models enable solid hypotheses that can be thoroughly tested. The hope is that use of this model could lead to an acceleration of therapies for brain dysfunction as well as offer a better way to study normal brain physiology.”

Kaplan and his team are looking into how they can make their tissue model more brain-like. In this recent report, the researchers demonstrated that they can modify their donut scaffold so that it consists of six concentric rings, each able to be populated with different types of neurons. Such an arrangement would mimic the six layers of the human brain cortex, in which different types of neurons exist.

As part of the funding agreement for the Tissue Engineering Resource Center, NIBIB requires that new technologies generated at the center be shared with the greater biomedical research community.

“We look forward to building collaborations with other labs that want to build on this tissue model,” said Kaplan.

Filed under brain tissue white matter gray matter brain function homeostasis neurons neuroscience science

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August 12, 2014

Target Identified For Rare Inherited Neurological Disease In Men

ucsdhealthsciences:

Scientists show bad androgen receptor impairs body’s ability to dispose of damaged cells

Researchers at University of California, San Diego School of Medicine have identified the mechanism by which a rare, inherited neurodegenerative disease causes often crippling muscle weakness in men, in addition to reduced fertility.

The study, published August 10 in the journal Nature Neuroscience, shows that a gene mutation long recognized as a key to the development of Kennedy’s disease impairs the body’s ability to degrade, remove and recycle clumps of “trash” proteins that may otherwise build up on neurons, progressively impairing their ability to control muscle contraction. This mechanism, called autophagy, is akin to a garbage disposal system and is the only way for the body to purge itself of non-working, misshapen trash proteins.

“We’ve known since the mid-1990s that Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are caused by the accumulation of misfolded proteins that should have been degraded, but cannot be turned over,” said senior author Albert La Spada, MD, PhD and professor of pediatrics, cellular and molecular medicine, and neurosciences. “The value of this study is that it identifies a target for halting the progression of protein build-up, not just in this rare disease, but in many other diseases that are associated with impaired autophagy pathway function.”

Of the 400 to 500 men in the U.S. with Kennedy’s disease, the slow but progressive loss of motor function results in about 15 to 20 percent of those with the disease becoming wheel-chair bound during later stages of the disease.

Kennedy’s disease, also known as spinal and bulbar muscular atrophy, is a recessive X-linked disease men inherit from their mother. Women don’t get the disease because they have two copies of the X chromosome. The genetic abnormality causes men to produce a mutant androgen receptor protein, which impairs the body’s sensitivity and response to male sex hormones, sometimes resulting in testicular atrophy and enlargement of male breasts.

In experiments with mice, scientists discovered that the mutant androgen receptor protein besides disrupting male reproductive biology also deactivates a protein called transcription factor EB (TFEB) that is believed to be a master regulator of autophagy in nerve and other cell types.

Specifically, the mutant androgen receptor protein in Kennedy’s disease binds to TFEB and blocks its ability to mediate the break-down and removal of non-working proteins and aggregated proteins.

“Our study tells us that if we can find a way to keep TFEB working, we likely can prevent this disease and others like it from progressing,” La Spada said. “We now have a target for new therapies to treat not only Kennedy’s disease, but also many more common neurological disorders.”

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August 12, 2014

Testosterone in Healthy Men Increases Their Brains’ Response to Threat

Testosterone, a steroid hormone, is well known to contribute to aggressive behavior in males, but the neural circuits through which testosterone exerts these effects have not been clear.

Prior studies found that the administration of a single dose of testosterone influenced brain circuit function. Surprisingly, however, these studies were conducted exclusively in women.

Researchers, led by Dr. Justin Carré, sought to rectify this gap by conducting a study of the effects of testosterone on the brain’s response to threat cues in healthy men.

They focused their attention on brain structures that mediate threat processing and aggressive behavior, including the amygdala, hypothalamus, and periaqueductal gray.

The researchers recruited 16 healthy young male volunteers, who completed two test days on which they received either testosterone or placebo. On both testing days, the men first received a drug that suppressed their testosterone. This step ensured that testosterone levels were similar among all study participants. The amount of testosterone administered in this study only returned testosterone levels to the normal range. Subjects then completed a face-matching task while undergoing a functional magnetic resonance imaging scan.

Data analyses revealed that, compared with placebo, testosterone increased reactivity of the amygdala, hypothalamus and periaqueductal grey when viewing angry facial expressions.

"We were able to show for the first time that increasing levels of testosterone within the normal physiological range can have a profound effect on brain circuits that are involved in threat-processing and human aggression," said Carré, Assistant Professor at Nipissing University.

"Understanding testosterone effects on the brain activity patterns associated with threat and aggression may help us to better understand the ‘fight or flight’ response in males that may be relevant to aggression and anxiety," commented Dr. John Krystal, Editor of Biological Psychiatry.

Expanding our knowledge of exactly how testosterone affects the male brain is particularly important, as testosterone augmentation has become increasingly promoted and aggressively marketed as a solution to reduced virility in aging men. Further work is indeed continuing, Carré said. “Our current work is examining the extent to which a single administration of testosterone influences aggressive and competitive behavior in men.”

(Source: elsevier.com)

Filed under testosterone brain activity aggression amygdala androgens emotion neuroscience science

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August 12, 2014

ucsdhealthsciences:

Novel Study Maps Infant Brain Growth In First Three Months of Life Using MRI Technology
Results may be key in identifying and treating earliest signs of neurodevelopmental disorders

A recent study conducted by researchers at the University of California, San Diego School of Medicine and the University of Hawaii demonstrates a new approach to measuring early brain development of infants, resulting in more accurate whole brain growth charts and providing the first estimates for growth trajectories of subcortical areas during the first three months after birth. Assessing the size, asymmetry and rate of growth of different brain regions could be key in detecting and treating the earliest signs of neurodevelopmental disorders, such as autism or perinatal brain injury.

The study will be published in JAMA Neurology on August 11.

For the first time, researchers used magnetic resonance imaging (MRI) of the newborn brain to calculate the volume of multiple brain regions and to map out regional growth trajectories during the infant’s first 90 days of life. The study followed the brain growth of full term and premature babies with no neurological or major health issues.

“A better understanding of when and how neurodevelopmental disorders arise in the postnatal period may help assist in therapeutic development, while being able to quantify related changes in structure size would likely facilitate monitoring response to therapeutic intervention. Early intervention during a period of high neuroplasticity could mitigate the severity of the disorders in later years,” said Dominic Holland, PhD, first author of the study and researcher in the Department of Neurosciences at UC San Diego School of Medicine.

For more than two centuries, clinicians have tracked brain growth by measuring the outside of the infant’s head with a measuring tape. The results are then plotted on a percentile chart to indicate if normal growth patterns exist. While the measurement is helpful for observing growth, it does not reveal if the individual structures within the brain are developing normally.

On average, researchers found the newborn brain grows one percent each day immediately following birth but slows to 0.4 percent per day by three months. In general for both sexes, the cerebellum, which is involved in motor control, grew at the highest rate, more than doubling volume in 90 days. The hippocampus grew at the slowest rate, increasing in volume by only 47 percent in 90 days, suggesting that the development of episodic memory is not as important at this stage of life.

“We found that being born a week premature, for example, resulted in a brain four to five percent smaller than expected for a full term baby. The brains of premature babies actually grow faster than those of term-born babies, but that’s because they’re effectively younger – and younger means faster growth,” said Holland. “At 90 days post-delivery, however, premature brains were still two percent smaller. The brain’s rapid growth rates near birth suggest that inducing early labor, if not clinically warranted, may have a negative effect on the infant’s neurodevelopment.”

The study also found that many asymmetries in the brain are already established in the early postnatal period, including the right hippocampus being larger than the left, which historically, has been suggested to occur in the early adolescent years. Cerebral asymmetry is associated with functions such as dexterity and language abilities.

Next steps involve continuing to make advances in the application of different MRI modalities to examine the newborn brain. MRI provides high quality images of different types of tissue and does not involve radiation, like computed tomography (CT). Future research will investigate how brain structure sizes at birth and subsequent growth rates are altered as a result of alcohol and drug consumption during pregnancy.

“Our findings give us a deeper understanding of the relationship between brain structure and function when both are developing rapidly during the most dynamic postnatal growth phase for the human brain,” said Holland.

Image courtesy of NMMG

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August 12, 2014

Study captures brain activity in children suffering emergence delirium

In a world-first, a newly published study has captured in detail the brain electrical activity in children as they emerge from anaesthesia, shedding light on why some are distressed and agitated when they wake up.

Researchers from Swinburne University of Technology together with colleagues from the Murdoch Childrens Research Institute (MCRI) were able to collect electroencephalography (EEG) data on children who exhibited emergence delirium.

Emergence delirium is a major risk associated with anaesthesia in children and occurs when patients wake up from anaesthesia in a delirious and disassociated state.

Swinburne Professor David Liley said PhD student Jessica Martin and staff at MCRI were able to record, with unprecedented fidelity, brain electrical activity from 60 children aged 5-15 years who emerged from anaesthesia some of whom went on to exhibit emergence delirium.

“This clinical phenomenon is prevalent in children aged six and under, with an estimated 10-30% exhibiting emergence delirium,” said Professor Liley.

Researchers found that the brain activity recorded just after stopping sevoflurane (a form of gas anaesthesia) in children exhibiting emergence delirium was substantially different to those children who woke up peacefully.

Associate Professor Andrew Davidson from MCRI said they discovered that children who wake up suddenly from a deeper plane of anaesthetic are more likely to develop the delirium.

“In contrast, the children who develop sleep like patterns on their EEG before they wake up are more likely to wake up peacefully.”

“Intriguingly, emergence delirium looks very much like the more severe form of night terror, which occurs when some pre-school children are disturbed during deep sleep.

“Our study suggests the EEG signatures and the mechanisms may indeed be similar between night terror and emergence delirium.

“Allowing children to wake up in a quiet and undisturbed environment should increase the likelihood that they go into a light sleep-like state after the anaesthetic and then wake up peacefully,” said Associate Professor Davidson.

The findings will have significant implications in both predicting those children who will go on to develop emergence delirium, as well as helping medical professionals better understand its causes in both children and adults.

The study, Alterations in the Functional Connectivity of Frontal Lobe Networks Preceding Emergence Delirium in Children, will appear in the October issue of the high profile clinical journal, Anesthesiology and is electronically available ahead of print.

(Source: swinburne.edu.au)

Filed under brain activity anesthesia emergence delirium children functional connectivity neuroscience science

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August 12, 2014

Medicinal oil reduces debilitating epileptic seizures associated with Glut 1 deficiency, trial shows

Two years ago, the parents of Chloe Olivarez watched painfully as their daughter experienced epileptic seizures hundreds of times a day. The seizures, caused by a rare metabolic disease that depleted her brain of needed glucose, left Chloe nearly unresponsive, and slow to develop.

Within hours, treatment with an edible oil dramatically reduced the number of seizures for then-4-year-old Chloe, one of 14 participants in a small UT Southwestern Medical Center clinical trial.

“Immediately we noticed fewer seizures. From the Chloe we knew two years ago to today, this is a completely different child. She has done amazingly well,” said Brandi Olivarez, Chloe’s mother.

For Chloe and the other trial participants who suffer from the disease called Glut1 deficiency (G1D), seizure frequency declined significantly. Most showed a rapid increase in brain metabolism and improved neuropsychological performance, findings that suggested the oil derived from castor beans called triheptanoin, ameliorated the brain glucose-depletion associated with this genetic disorder, which is often undiagnosed.

“This study paves the way for a medical food designation for triheptanoin, thus significantly expanding therapeutic options for many patients,” said Dr. Juan Pascual, Associate Professor of Neurology and Neurotherapeutics, Physiology, and Pediatrics at UT Southwestern and lead author of a study on the findings, published in JAMA Neurology.

For the estimated 38,000 Americans suffering from this disease, the only proven treatment has been a high-fat ketogenic diet, which only works for about two-thirds of patients. In addition, this diet carries long-term risks, such as development of kidney stones and metabolic abnormalities.

Based on the results of this trial, triheptanoin appears to work as efficiently as the ketogenic diet; however, more research needs to be done before the oil is made available as a medical food therapy, researchers said.

“Triheptanoin byproducts produced in the liver and also in the brain refill brain chemicals that we found are preferentially diminished in the disorder, and this effect is precisely what defines a medical food rather than a drug,” said Dr. Pascual, who heads UT Southwestern’s Rare Brain Disorders Program, maintains an appointment in the Eugene McDermott Center for Human Growth and Development, and holds The Once Upon a Time Foundation Professorship in Pediatric Neurologic Diseases.

The oil, approved for use in research only, is an ingredient in some cosmetic products and is added to butter in some European countries. It is not commercially available in the U.S. for clinical use.

Triheptanoin’s success as an experimental treatment for other metabolic diseases, along with preclinical success in G1D mice, led Dr. Pascual and his trial collaborator, Dr. Charles Roe, Clinical Professor of Neurology and Neurotherapeutics, to first conceive the idea and then launch this trial for G1D patients. The 14 pediatric and adult patients in the study consumed varying amounts of the oil, based on their body weight, four times a day. Given the trial’s success, Dr. Pascual plans further research to refine the optimal dosage toward the goal of facilitating medical food designation of triheptanoin as a new G1D treatment.

While some trial participants reported mild stomach upset as a side effect, for Chloe the oil has been a miracle medicine without negative effects. Her parents, Brandi and Josh Olivarez of Waco, Texas, continue to be amazed by her progress.

“Before, she was having so many seizures a day that she couldn’t even talk. Now she sings all the time, she can eat whatever she wants, and her speech is greatly improved. She still has some learning delays, but has come a long way,” said Mrs. Olivarez.

Many Glut1 patients suffer from movement disorders that limit their physical capabilities, but that does not appear to be the case with Chloe. As for the seizures, she still has minor ones occasionally, but they are not debilitating.

“She is now able to run a solid mile without stopping. This would not have been possible without the oil,” Mrs. Olivarez said. “Before, she had almost no muscle tone, was lethargic and had a very wide gait due to trying to balance herself while walking, which was very tiring for her.”

To better understand this disease, UT Southwestern established a patient-completed registry to track G1D incidence and what treatments work or do not work for those registered.

Filed under glut1 deficiency epileptic seizures triheptanoin cerebral metabolism glucose neuroscience science

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August 12, 2014

Important advance in brain mapping and memory

“When a tiger starts to move towards you, you need to know whether it is something you are actually seeing or whether it’s just something that you remember or have imagined,” says Prof. Julio Martinez-Trujillo of McGill’s Department of Physiology. The researcher and his team have discovered that there is a clear frontier in the brain between the area that encodes information about what is immediately before the eyes and the area that encodes the abstract representations that are the product of our short-term memory or imagination. It is an important advance in brain mapping and opens the doors to further research in the area of short-term memory.

These finding, which are described in an article just published in Nature Neuroscience, resolve a question that has occupied neuroscientists for years. Namely that of how and where exactly in the brain the visual information coming from our eyes is first transformed into short-term memories. “We found that while one area in the brain processes information about what we are currently seeing, an area right beside it stores the information in short-term memory,” says McGill PhD student Diego Mendoza-Halliday, first author of the article. “What is so exciting about this finding is that until now, no one knew the place where visual information first gets transformed into short-term memory.”

The researchers arrived at this conclusion by measuring the neuronal activity in these two areas in the brains of macaques as they first looked at, and then after a short time (1.2 - 2 seconds) remembered, a random sequence of dots moving across a computer screen like rainfall. What surprised Martinez-Trujillo and his team was how clearly demarcated the divide was between the activities and functions of the two brain areas, and this despite the fact that they lie side-by-side.

“It is rare to find this kind of sharp boundary in biological systems of any kind,” says Martinez-Trujillo. “Most of the time, when you look at the function of different brain areas, there is more of a transitional zone, more grey and not such a clear border between black and white. I think the evolutionary reason for this clear frontier is that it helped us to survive in dangerous situations.”

The discovery comes after five years spent by Martinez-Trujillo and his team doing research in the area. Despite this fact, he acknowledges that there was a certain amount of serendipity, and a lot of technological help involved in being able to capture a signal that travels for 3 milliseconds and fires synapses in neurons that lie right beside one another.

Martinez-Trujillo and his team continue to work on mapping the receptors and connectivity between these two areas of the brain. But what is most important for him is to try and relate this discovery to schizophrenia and other diseases that involve hallucinations, and in order to do so he is working with a psychiatrist at Montreal’s Douglas Hospital.

(Image: Bigstock)

Filed under STM visual cortex brain activity visual memory working memory neuroscience science