Posts tagged neuroscience

ScienceDaily (Mar. 21, 2012) — Scientists at the Stanford University School of Medicine have shown for the first time how brain function differs in people who have math anxiety from those who don’t.

A series of scans conducted while second- and third-grade students did addition and subtraction revealed that those who feel panicky about doing math had increased activity in brain regions associated with fear, which caused decreased activity in parts of the brain involved in problem-solving.

"The same part of the brain that responds to fearful situations, such as seeing a spider or snake, also shows a heightened response in children with high math anxiety," said Vinod Menon, PhD, the Stanford professor of psychiatry and behavioral sciences who led the research.

In their new study, published online March 20 in Psychological Science, a journal of the Association for Psychological Science, Menon’s team performed functional magnetic resonance imaging brain scans on 46 second- and third-grade students with low and high math anxiety. Outside the fMRI scanner, the children were assessed for math anxiety with a modified version of a standardized questionnaire for adults, and also received standard intelligence and cognitive tests.

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ScienceDaily (Mar. 21, 2012) — Healthy individuals who carry a gene variation linked to an increased risk of autism have structural differences in their brains that may help explain how the gene affects brain function and increases vulnerability for autism. The results of this innovative brain imaging study are described in an article in the groundbreaking neuroscience journal Brain Connectivity, a bimonthly peer-reviewed publication from Mary Ann Liebert, Inc. The article is available free online at the Brain Connectivity website.

"This is one of the first papers demonstrating a linkage between a particular gene variant and changes in brain structure and connectivity in carriers of that gene," says Christopher Pawela, PhD, Co-Editor-in-Chief and Assistant Professor, Medical College of Wisconsin. "This work could lead to the creation of an exciting new line of research investigating the impact of genetics on communication between brain regions."

Although carriers of the common gene variant CNTNAP2 — identified as an autism risk gene — may not develop autism, there is evidence of differences in brain structure that may affect connections and signaling between brain regions. These disruptions in brain connectivity can give rise to functional abnormalities characteristic of neuropsychological disorders such as autism.

Emily Larson Dennis, Neda Jahanshad, Jeffrey D Rudie, Jesse A Brown, Kori Johnson, Katie McMahon, Greig de Zubicaray, Grant Montgomery, Nicholas Martin, Margaret Wright, Susan Bookheimer, Mirella Dapretto, Arthur Toga, Paul Thompson. Altered Structural Brain Connectivity in Healthy Carriers of the Autism Risk Gene, CNTNAP2. Brain Connectivity, 2012; 120229030236004 DOI: 10.1089/brain.2011.0064

Source: Science Daily

ScienceDaily (Mar. 21, 2012) — Why does inhaling anesthetics cause unconsciousness? New insights into this century-and-a-half-old question may spring from research performed at the National Institute of Standards and Technology (NIST). Scientists from NIST and the National Institutes of Health have found hints that anesthesia may affect the organization of fat molecules, or lipids, in a cell’s outer membrane — potentially altering the ability to send signals along nerve cell membranes.

"A better fundamental understanding of inhaled anesthetics could allow us to design better ones with fewer side effects," says Hirsh Nanda, a scientist at the NIST Center for Neutron Research (NCNR). "How these chemicals work in the body is a scientific mystery that stretches back to the Civil War."

At the turn of the 20th century, doctors suspected inhaled anesthetics had some effect on cell membranes, an animal cell’s outer boundary. Despite considerable investigation, however, no one was able to demonstrate that anesthetics produced changes in the physical properties of membranes large enough to cause anesthesia. But eventually, understanding of membrane function grew more refined as scientists learned more about ion channels.

Ion channels — large proteins embedded in the relatively small lipid molecules forming the membrane — are responsible for conducting electrical impulses along nerve cells in the brain and throughout our body. By a few decades ago, the prevailing theory held that inhaled anesthetics directly interacted with these protein channels, affecting their behavior in some fashion. But no one could find a single type of ion channel that reacted to anesthetics in a way pivotal enough to settle the matter, and the question remained open.

"That’s where we picked up the thread," says Nanda. "We had been looking at how different types of lipid molecules affect ion channels."

While a cell membrane is a highly fluid film made of many different kinds of lipid molecules, the region immediately surrounding an ion channel often consists of a single type of lipids that form a sort of “raft” that is more ordered and less fluid then the rest of the membrane. When the team heard other researchers had found that disrupting these lipid rafts could affect a channel’s function, they put to work their own previous experience working with the channels.

"We decided to test whether inhaled anesthetics could have an effect on rafts in model cell membranes," Nanda says. "No one had thought to ask the question before."

Using the NCNR’s neutron and X-ray diffraction devices as their microscope, the team explored how a model cell membrane responded to two chemicals — inhaled anesthetic, and another that has many of the same chemical properties as anesthetic but does not cause unconsciousness. Their finding showed a distinct difference in the way the lipid rafts responded: Exposing the membranes to an anesthetic caused the rafts to grow disorderly, freely mixing its lipids with the surrounding membrane, but the second chemical had a dramatically smaller effect.

While Nanda says the discovery does not answer the question definitively, he and his co-authors are following up with other experiments that could clarify the issue. “We feel the discovery has opened up an entirely new line of inquiry into this very old puzzle,” he says.

Source: Science Daily

March 21, 2012

Scientists from Germany discovered new functions of brain regions that are responsible for seeing movement.

When observing a fly buzzing around the room, we should have the impression that it is not the fly, but rather the space that lies behind it that is moving. After all, the fly is always fixed in our central point of view. But how does the brain convey the impression of a fly in motion in a motionless field? With the help of functional magnetic resonance imaging (fMRI) scientists from the Werner Reichardt Centre for Integrative Neuroscience and the Max Planck Institute for Biological Cybernetics in Tübingen have identified two areas of the brain that compare the movements of the eye with the visual movements cast onto the retina so as to correctly perceive objects in motion.

The two areas of the brain that are particularly good at reacting to external movements, even during eye movements, are known as V3A and V6. They are located in the upper half in the posterior part of the brain. Area V3A shows a high degree of integration: it reacts to movements around us regardless of whether or not we follow the moving object with our eyes. But the area does not react to visual movements on the retina when eye movements produce them. Area V6 has similar characteristics. In addition, it can perform these functions when we are moving forwards. The calculations the brain has to perform are more complicated in this case: the three-dimensional, expanding forward movement is superimposed onto the two-dimensional lateral movements that are caused by eye movements.

The scientists Elvira Fischer and Andreas Bartels from the Werner Reichardt Centre for Integrative Neuroscience and the Max Planck Institute for Biological Cybernetics have investigated these areas with the help of functional magnetic resonance imaging (fMRI). fMRI is a procedure that can measure brain activity based on local changes in blood flow and oxygen consumption. Participants in the study were shown various visual scenarios whilst undergoing fMRI scanning. For example, they had to follow a small dot with their eyes while it moved across a screen from one side to the other. The patterned background was either stationary or moved at varying speeds, sometimes slower, faster or at the same speed as the dot. Sometimes the dot was stationary while only the background moved. In a total of six experiments the scientists measured brain activity in more than a dozen different scenarios. From this they have been able to discover that V3A and V6, unlike other visual areas in the brain, have a pronounced ability to compare eye movements with the visual signals on the retina. “I am especially fascinated by V3A because it reacts so strongly and selectively to movements in our surroundings. It sounds trivial, but it is an astonishing capability of the brain”, explains Andreas Bartels, project leader of the study.

Whether it is ourselves who move or something else in our surroundings is a problem about which we seldom think, since at the subconscious level our brain constantly calculates and corrects our visual impression. Indeed, patients who have lost this ability to integrate movements in their surroundings with their eye movements can no longer recognize what it is that ultimately is moving: the surroundings or themselves. Every time they move their eyes these patients feel dizzy. Studies such as this bring us one step closer to an understanding of the causes of such illnesses.

Provided by Max-Planck-Gesellschaft

Source: medicalxpress.com

March 21, 2012

Amateurs have a new tool for conducting simple neuroscience experiments in their own garage: the SpikerBox.

As reported in the Mar. 21 issue of the open access journal PLoS ONE, the SpikerBox lets users amplify and listen to neurons’ electrical activity – like those in a cockroach leg or cricket torso – and is appropriate for use in middle or high school educational programs, or by amateurs.

The work was a project from Backyard Brains, a start-up company focused on developing neuroscience educational resources. In the paper, the authors, Timothy Marzullo and Gregory Gage, describe a sample experiment using a cockroach leg stuck with two needles and monitoring the electrical signals. They also provide instructions for using the SpikerBox to answer specific experimental questions, like how neurons carry information about touch, how the brain tells muscles to move, and how drugs affect neurons, and an online portal provides further instructional materials. These are just a few examples of the many ways this tool can be used.

"Our mission is to lower the barrier-to-entry for students interested in learning about the brain. We hope our manuscript finds its way into the hands of high school teachers around the world", says Dr. Marzullo.

Provided by Public Library of Science

Source: medicalxpress.com

March 21, 2012

(Medical Xpress) — People who lose their sight at a later stage in life have a greater spatial awareness than if they were born blind, according to scientists at Queen Mary, University of London.

The study, published in the journal Neuroscience and Biobehavioral Reviews, examined research which looked at the spatial skills of sighted and blind people and found that some spatial tasks need visual experience.

Co-author on the study, Dr. Michael Proulx from Queen Mary’s School of Biological and Chemical Sciences, said: “Numerous studies have tested how humans use vision for knowing the spatial locations of things yet few have examined the other senses and whether people with a visual impairment use the same strategies.

“In reviewing research already available, we found visual experience is necessary for the brain to develop the ability to process multisensory information. We use vision and the other senses to create a mental map of where objects are in relation to other objects and the environment.

“Our findings suggest that there is a sensitive period during which visual experience is necessary for the brain to develop those neurons that can represent the world in this way.”

Lead author Dr. Achille Pasqualotto, also from Queen Mary’s School of Biological and Chemical Sciences, said: “Blindness reveals how well humans can function using the remaining senses, even in a world designed by sighted people for sighted people.

“The brain develops spatial abilities that relate an object’s location to the individual. This makes sense given that a visually impaired person does not see objects at a distance in an environment, but instead acquires their location by personally approaching and identifying them.”

The team is building on their findings now by testing sighted and blind people on a variety of spatial tasks that will explicitly test these findings.

They hope this research will not only reveal the psychological and neural basis for spatial cognition, but also translate into better services for blind persons, such as the development of better navigational tools.

Dr. Proulx said: “We are actively recruiting blind people to participate in our research and we are particularly keen to involve people who have been blind since birth, yet people who lost vision later in life would be welcome to contact us too.”

Provided by Queen Mary, University of London

Source: medicalxpress.com

March 21, 2012

Research at the University of Calgary’s Hotchkiss Brain Institute (HBI) has demonstrated the novel expression of an ion channel in Purkinje cells – specialized neurons in the cerebellum, the area of the brain responsible for movement. Ray W. Turner, PhD, Professor in the Department of Cell Biology & Anatomy and PhD student Jordan Engbers and colleagues published this finding in the January edition of the journal Proceedings of the National Academy of Sciences (PNAS).

This research identifies for the first time that an ion channel called KCa3.1 that was not previously believed to be expressed in the brain is actually present in Purkinje cells. In addition, these researchers demonstrate the mechanism by which this ion channel allows Purkinje cells to filter sensory input in order to coordinate the body’s movements.

The discovery was unexpected, as Engbers explains, “we didn’t specifically go looking for this channel. A lot of time was spent trying to identify the source for an electrical current that we were observing and we finally found ourselves asking ‘what evidence is there that KCa3.1 isn’t in the brain?’ So we ran some tests and all the pieces really fell into place.”

In the cerebellum, sensory input activates neurons called Purkinje cells that have to filter the information and respond only to relevant inputs to produce an appropriate movement response. Although this function of Purkinje cells has been well documented, Engbers and Turner take our understanding a step further by demonstrating that the KCa3.1 ion channel plays a key part in this process - acting as a gatekeeper to filter the enormous amount of incoming information.

As Turner explains, “these cells receive hundreds of thousands of signals every second from the body’s sensory systems. KCa3.1 then allows the cells to filter out the background noise and respond to only the three or four inputs that are particularly relevant”.

Engbers further describes the mechanism by which KCa3.1 filters out the unwanted information, “these channels are activated by an influx of calcium, which generates an inhibitory influence until the correct input is detected. Once the appropriate input is detected, the Purkinje cell responds with a burst of nerve impulses, which in turn initiates the proper motor response.”

This research fills a substantial gap in understanding how neurons in the cerebellum process information. Engbers and Turner expect that continued research will identify KCa3.1 in other areas of the brain and that it will be responsible for several still unexplained phenomena observed in neuronal recordings.

"What we have found will help us understand how the cerebellum functions normally. Now that we have shown the scientific community this new information, we expect that it will become clear that KCa3.1 plays a much wider role in brain function," says Engbers.

Provided by University of Calgary 

Source: medicalxpress.com

March 21, 2012

Researchers at Weill Cornell Medical College have developed a computer program that has tracked the manner in which different forms of dementia spread within a human brain. They say their mathematic model can be used to predict where and approximately when an individual patient’s brain will suffer from the spread, neuron to neuron, of “prion-like” toxic proteins — a process they say underlies all forms of dementia.

Their findings, published in the March 22 issue of Neuron, could help patients and their families confirm a diagnosis of dementia and prepare in advance for future cognitive declines over time. In the future — in an era where targeted drugs against dementia exist — the program might also help physicians identify suitable brain targets for therapeutic intervention, says the study’s lead researcher, Ashish Raj, Ph.D., an assistant professor of computer science in radiology at Weill Cornell Medical College.

"Think of it as a weather radar system, which shows you a video of weather patterns in your area over the next 48 hours," says Dr. Raj. "Our model, when applied to the baseline magnetic resonance imaging scan of an individual brain, can similarly produce a future map of degeneration in that person over the next few years or decades.

"This could allow neurologists to predict what the patient’s neuroanatomic and associated cognitive state will be at any given point in the future. They could tell whether and when the patient will develop speech impediments, memory loss, behavioral peculiarities, and so on," he says. "Knowledge of what the future holds will allow patients to make informed choices regarding their lifestyle and therapeutic interventions.

"At some point we will gain the ability to target and improve the health of specific brain regions and nerve fiber tracts," Dr. Raj says. "At that point, a good prediction of a subject’s future anatomic state can help identify promising target regions for this intervention. Early detection will be key to preventing and managing dementia." 

Tracking the Flow of Proteins

The computational model, which Dr. Raj developed, is the latest, and one of the most significant, validations of the idea that dementia is caused by proteins that spread through the brain along networks of neurons. It extends findings that were widely reported in February that Alzheimer’s disease starts in a particular brain region, but spreads further via misfolded, toxic “tau” proteins. Those studies, by researchers at Columbia University Medical Center and Massachusetts General Hospital, were conducted in mouse models and focused only on Alzheimer’s disease.

In this study, Dr. Raj details how he developed the mathematical model of the flow of toxic proteins, and then demonstrates that it correctly predicted the patterns of degeneration that results in a number of different forms of dementia.

He says his model is predicated on the recent understanding that all known forms of dementia are accompanied by, and likely caused by, abnormal or “misfolded” proteins. Proteins have a defined shape, depending on their specific function — but proteins that become misshapen can produce unwanted toxic effects. One example is tau, which is found in a misfolded state in the brains of both Alzheimer’s patients and patients with frontal temporal dementia (FTD). Other proteins, such as TDP43 and ubiquitin, are also found in FTD, and alpha synuclein is found in Parkinson’s disease.

These proteins are called “prion-like” because misfolded, or diseased, proteins induce the misfolding of other proteins they touch down a specific neuronal pathway. Prion diseases (such as mad cow disease) that involve transmission of misfolded proteins are thought to be infectious between people. “There is no evidence that Alzheimer’s or other dementias are contagious in that way, which is why their transmission is called prion-like.”

Simple Explanation for Clinically Observed Patterns of Dementia

Dr. Raj calls his model of trans-neuronal spread of misfolded proteins “very simple.” It models the same process by which any gas diffuses in air, except that in the case of dementias the diffusion process occurs along connected neural fiber tracts in the brain.

"This is a common process by which any disease-causing protein can result in a variety of dementias," he says.

The model identifies the neural sub-networks in the brain into which misfolded proteins will collect before moving on to other brain areas that are connected by networks of neurons. In the process the proteins alter normal functioning of all brain areas they visit.

"What is new and really quite remarkable is the network diffusion model itself, which acts on the normal brain connectivity network and manages to reproduce many known aspects of whole brain disease patterns in dementias," Dr. Raj says. "This provides a very simple explanation for why different dementias appear to target specific areas of the brain."

In the study, he was able to match patterns from the diffusion model, which traced protein disbursal in a healthy brain, to the patterns of brain atrophy observed in patients with either Alzheimer’s disease or FTD. This degeneration was measured using MRI and other tools that could quantify the amount of brain volume loss experienced in each region of the patient’s brain. Co-author Amy Kuceyeski, Ph.D., a postdoctoral fellow who works with Dr. Raj, helped analyze brain volume measurements in the diseased brains.

"Our study demonstrates that such a spreading mechanism leads directly to the observed patterns of atrophy one sees in various dementias," Dr. Raj says. "While the classic patterns of dementia are well known, this is the first model to relate brain network properties to the patterns and explain them in a deterministic and predictive manner."

Provided by New York- Presbyterian Hospital

Source: medicalxpress.com

March 21, 2012

Alzheimer’s disease and other forms of dementia may spread within nerve networks in the brain by moving directly between connected neurons, instead of in other ways proposed by scientists, such as by propagating in all directions, according to researchers who report the finding in the March 22 edition of the journal Neuron.

Led by neurologist and MacArthur Foundation “genius award” recipient William Seeley, MD, from the UCSF Memory and Aging Center, and post-doctoral fellow Helen Juan Zhou, PhD, now a faculty member at Duke-NUS Graduate Medical School in Singapore, the researchers concluded that a nerve region’s connectedness to a disease hot spot trumps overall connectedness, spatial proximity and loss of growth-factor support in predicting its vulnerability to the spread of disease in some of the most common forms of dementia, including Alzheimer’s disease.

The finding, based on new magnetic resonance imaging research (MRI), raises hopes that physicians may be able to use MRI to predict the course of dementias – depending on where within an affected network degenerative damage is first discovered – and that researchers may use these predicted outcomes to determine whether a new treatment is working. Network modeling combined with functional MRI might serve as an intermediate biomarker to gauge drug efficacy in clinical trials before behavioral changes become measurable, according to Seeley.

"Our next goal is to further develop methods to predict disease progression, using these models to create a template for how disease will progress in the brain of an affected individual," Seeley said. "Already this work suggests that if we know the wiring diagram in a healthy brain, we can predict where the disease is going to go next. Once we can predict how the network will change over time we can predict how the patient’s behavior will change over time and we can monitor whether a potential therapy is working."

The new evidence suggests that different kinds of dementias spread from neuron to neuron in similar ways, even though they act on different brain networks, according to Seeley. Seeley’s previous work and earlier clinical and anatomical studies showed that the patterns of damage in the dementias are linked to particular networks of nerve cells, but until now scientists have found it difficult to evaluate in humans their ideas about how this neurodegeneration occurs.

In the current study, the researchers modeled not only the normal nerve network that can be affected by Alzheimer’s disease, but also those networks affected by frontotemporal dementia (FTD) and related disorders, a class of degenerative brain diseases identified by their devastating impact on social behaviors or language skills.

The scientists mapped brain connectedness in 12 healthy people. Then they used data from patients with the five different diseases to map and compare specific regions within the networks that are damaged by the different dementias.

"For each dementia, we looked at four ideas that scientists often bring up to explain how dementia might target brain networks," Seeley said. "The different proposed mechanisms lead to different predictions about how a region’s place in the healthy network affects its vulnerability to disease."

In the “nodal stress” hypothesis, small regions within the brain that serve as hubs to carry heavy signaling traffic would undergo wear and tear that gives rise to or worsens disease. In the “trophic failure” mechanism, breakdowns in connectivity would disrupt transport through the network of growth factors needed to maintain neurons. In the “shared vulnerability” mechanism, specific genes or proteins common to neurons in a network would make them more susceptible to disease. But predictions from the “trans-neuronal spread” mechanism model best fit the network connectivity maps constructed by the researchers.

"The trans-neuronal spread model predicts that the more closely connected a region is to the node of disease onset – which we call the epicenter – then the more vulnerable that region will be once the disease begins to spread," Seeley said. "It’s as if the disease is emanating from a point of origin, but it can reach any given target faster if there is a stronger connection."

The scientists tracked and analyzed linkages within nerve networks that the dementias target. They used a technique called functional connectivity MRI to measure and spatially represent activity in specific regions of key networks in the brains of the healthy subjects. The MRI readout allowed the researchers to model each region within the network as a distinct but interconnected node. They ranked the nodes that most consistently fired together as being the most closely connected.

Across the five diseases investigated in the study, trans-neuronal spread was the proposed mechanism for which the data best matched the predictions. Previous studies of animals and cells in the laboratory also support the idea that disease-related proteins can spread from an affected neuron to other neurons via intercellular connections.

For more than three decades researchers have been noticing that regions affected by Alzheimer’s disease are connected by axons that branch between and connect neurons, Seeley said. Trans-neuronal spread is a proven hallmark of certain rare neurodegenerative diseases – such as Creutzfeldt-Jakob disease – that are propagated by misfolded cell-surface proteins called prions, which induce neighboring proteins to change shape, aggregate and wreak havoc.

While Alzheimer’s disease and FTD are not considered infectious, abnormal protein structures also are implicated in these common dementias. Recent experiments in which researchers transplanted post-mortem, human brain extracts from dementia patients into genetically modified mice have resulted in disease, Seeley said, “But it is difficult to explore these ideas in humans, and we wanted to begin to bridge this knowledge gap.”

Provided by University of California - San Francisco

Source: medicalxpress.com 

March 21, 2012

What characterizes many people with depression, schizophrenia and some other mental illnesses is anhedonia: an inability to gain pleasure from normally pleasurable experiences.

This image shows VTA dopamine neurons (in red) and VTA GABA fibers (in green). Credit: Stuber Lab, UNC-Chapel Hill.

Exactly why this happens is unclear. But new research led by neuroscientists at the University of North Carolina at Chapel Hill School of Medicine may have literally shined a light on the answer, one that could lead to the discovery of new mental health therapies. A report of the study appears March 22 in the journal Neuron.

The study used a combination of genetic engineering and laser technology to manipulate the wiring of a specific population of brain cells deep in a portion of a midbrain area that’s known to promote behavioral responses to reward.

"For many years it’s been known that dopamine neurons in the ventral midbrain, the ventral tegmental area, or VTA, are involved in reward processing and motivation. For example, they’re activated during exposure to drugs of abuse and to naturally rewarding experiences," said study lead author Garret D. Stuber, PhD, assistant professor in the departments of Psychiatry and Cell and Molecular Physiology, and the UNC Neuroscience Center.

"The major focus in our lab is to determine what other sorts of neural circuits or genetically defined neural populations might be modulating the activity of those neurons, whether it’s increasing or decreasing their activity," Stuber said. "In our study we found that activation of the nearby VTA GABAergic neurons directly inhibit the function of dopamine neurons, which is something that’s never been shown before."

In the past, researchers have tried to get a glimpse into the inner workings of the brain using electrical stimulation or drugs, but those techniques couldn’t quickly and specifically change only one type of cell or one type of connection. But optogenetics, a technique that emerged about six years ago, can. 

In this study, the scientists used a transgenic animal with a foreign gene that has been inserted into its genome to express a bacterial enzyme that can cause DNA recombination only in GABA neurons and not dopamine cells. Using a gene transfer method developed at UNC and with the animal anesthetized, the Stuber team transferred light-sensitive proteins called “opsins” – derived from algae or bacteria that need light to grow – into the VTA, targeting GABA cells. The presence of these foreign opsins in GABA neurons allows researchers to excite or inhibit them by pumping light from a laser into brain tissue.

The animals were then tested in different reward situations, simple tasks in which they were trained to associate a cue with a sugar water reward from a bottle or were given the opportunity to drink the reward by “free licking,” where they could drink as much as they want.

Then, via optical fibers, the researchers shined laser beams onto the genetically manipulated GABA neurons, activating them for 5 seconds during the cue period followed by reward. And on another day, they activated the neurons during reward consumption, when the animals were actively engaged in drinking the sugar water.

"And what we saw when we activated the cells during the cue period, or reward anticipation, it didn’t do anything to the behavioral response at all; they showed no difference compared to non-stimulated animals," Stuber explained.

"And when they were actively engaging with the sucrose, we did see we could disrupt their reward consumption when we activated those cells. They immediately disengaged from drinking, stopped drinking the sucrose solution. And when the stimulus stopped, they would then return back and continue to drink it again."

During the “free licking” sessions, optical stimulation of GABA neurons resulted in disruption of sucrose consumption. The animals stopped drinking.

Using sophisticated electrophysiology and cell chemistry measures, the study team could monitor the activity of the GABA and dopamine neurons. They found a direct link between GABA activation and dopamine suppression.

"So basically, it appears that these GABA neurons located in the VTA are just microns away from dopamine and are negative regulators of dopamine function," Stuber proposes.

"When they become active, their basic job is to suppress dopamine release. A dysfunction in these GABA neurons might potentially underlie different aspects of neuropsychiatric illness, such as depression. Thus, we could think of them as a new physiological target for various aspects of neuropsychiatric diseases."

Provided by University of North Carolina School of Medicine