Posts tagged brain

ScienceDaily (June 26, 2012) — Magnetic fields generated by microscopic devices implanted into the brain may be able to modulate brain-cell activity and reduce symptoms of several neurological disorders. Micromagnetic stimulation appears to generate the kind of neural activity currently elicited with electrical impulses for deep brain stimulation (DBS) — a therapy that can reduce symptoms of Parkinson’s disease, other movement disorders, multiple sclerosis and chronic pain — and should avoid several common problems associated with DBS, report Massachusetts General Hospital investigators.

"We have shown that fields generated by magnetic coils small enough to be implanted into the central nervous system can be used to modulate the activity of neurons, potentially leading to a new generation of neural prosthetics that are safer and possibly more effective than conventional electrical stimulation devices," says Giorgio Bonmassar, PhD, of the Martinos Center for Biomedical Imaging at MGH, co-lead author of the report in the online journal Nature Communications.

DBS involves implantation of small electrodes called leads into structures deep within the brain. The leads, connected to a battery-operated power source implanted into the abdomen, generate electrical signals that modulate neural activity at sites that vary depending on the condition being treated. DBS has successfully alleviated symptoms in patients not helped by other therapies, but it does have limitations. Magnetic resonance imaging (MRI) can cause metallic DBS implants to heat up and damage adjacent brain tissue, which limits the use of MRI in these patients. In addition, the presence of DBS implants typically elicits an immune system response, leading to scarring around the implant that can block the electrical signal.

Magnetic stimulation has been used to diagnose and treat neurological disorders for two decades, but until now it has required the use of large hand-held coils that generate fields from outside the skull, limiting the brain structures that can be stimulated and the accuracy with which a signal can be delivered. The current study was designed to investigate the potential of much smaller magnetic coils to generate the kind of neural activity produced by DBS, exploring a concept first developed by Bonmassar. The investigators first developed a computational simulation that verified that magnetic coils 1 millimeter long and .5 mm in diameter would generate magnetic and electrical fields that should stimulate neuronal activity.

The research team then tested whether a commercially available coil of that size, coated with a plastic material, would activate neurons in retinal tissue. Positioned right above retinal tissue and either parallel or perpendicular to the tissue surface, the coil generated fields that successfully elicited neuronal signals in retinal cells. How the coil was positioned relative to the retinal surface produced significant differences in the physiologic responses. When the coil was oriented parallel to the retina, the induced field appeared to activate retinal bipolar cells, which transmit signals from the light-sensing photoreceptors to retinal ganglion cells. A coil oriented perpendicular to the retina produced responses indicative of ganglion cell activation.

"These differences suggest that, by modifying the geometry of the coil, we may be able to selectively target populations of neurons and minimize the effects on non-targeted cells," says Shelley Fried, PhD, of the MGH Department of Neurosurgery, corresponding author of the Nature Communications report. “By sizing and orienting the coil appropriately to any given population of central nervous system neurons, we should be able to either activate or avoid activation of that population.

"This study provides a proof of concept that small coils can activate neurons, and much work still needs to be done," he adds. "We need to explore how to optimize coil properties and then evaluate the devices in animal models. We also hope to explore the use of these coils in non-DBS applications, including cardiovascular procedures such as heart muscle pacing." Fried is an instructor in Surgery and Bonmassar an assistant professor of Radiology at Harvard Medical School.

Source: Science Daily

26 June 12 | By Liat Clark

A UK mathematician has made a public appeal for people to phone a dedicated number so data can be gathered to hone a tool that can diagnose Parkinson’s disease by analysing voice patterns.

Image: Shutterstock

Max Little, a research fellow at the Massachusetts Institute of Technology, made the announcement during the opening of the TEDGlobal conference in Edinburgh, 25 June. While studying at Oxford University, Little developed an algorithm that identifies the unique characteristics present in the voice of a Parkinson’s Disease sufferer. He setup the Parkinson’s Voice Initiative in order to improve upon the machine learning system — the algorithm is built to adapt when new information is introduced and, by widening the pool (it’s hoped, with 10,000 phone calls form the public), it should become a more accurate diagnosis tool, able to identify specific symptoms amid numerous variants of speech.

"This raises a very interesting possibility," Little says in a promotional video. "If we could use the entire existing telephone network then we could scale up the screening of Parkinson’s disease to the entire population, and do it at very minimal cost."

Other than the UK, there are phone numbers on the Parkinson’s Voice Initiative website for people in the US, Brazil, Mexico, Spain, Argentina and Canada. Parkinson’s sufferers and non-sufferers are both encouraged to call in anonymously. The calls should only last around three minutes. By getting non-sufferers to call in, the system can learn to weed out and discard unnecessary voice patterns, such as those brought on by a cold or heavy smoking.

Around 70-90 percent of sufferers report instances of vocal impairment following the onset of the disease. Little’s proposal therefore presents opportunities for widespread remote diagnosis.

He first presented the diagnosis tool’s successful testing in a paper published earlier this year in the IEEE Transactions journal. Little and co-author Athanasios Tsanas explained how 43 candidates were asked to hold one sound frequency for as long as possible. They collected 263 data samples in this way, and from this extracted 132 different vocal impairments. Using only ten of these recorded impairments, the algorithm could diagnose Parkinson’s speech markers accurately 99 percent of the time. The system is trained to identify the anomalies in the speech.

By collating more data in the future, the range of these vocal features could be widened, lessening the margin of error even more.

The paper suggests that in the future, data could be collected using Intel’s At-Home Testing Device, a telemonitoring system. It would then be sent to a clinic where the algorithm processes it and maps out the speech, identifying markers on the Unified Parkinson’s Disease Rating Scale (UPDRS) so that the severity of the illness is known. In this way, the system could not only be used to diagnose, but to monitor the progression of the disease.

Voice recognition could be a cheap and efficient alternative to having patients’ head to their GP for a twenty-minute diagnosis session. There is currently no simple diagnosis tool — no blood test that can identify Parkinson’s — and vocal tremors, breathiness and reduced speech volume are some of the first symptoms recorded in nearly all patients. These can be very subtle at the start, however, and systems such as Little’s could conceivably pick up the slightest abnormal intonation.

Parkinson’s Disease is the second most common neurodegenerative disorder after Alzheimer’s and, since it can only be treated with drugs or surgery and cannot be cured, early diagnosis can massively effect an individual’s quality of life.

Source: wired.co.uk

ScienceDaily (June 26, 2012) — Researchers have long been interested in discovering the ways that human brains represent thoughts through a complex interplay of electrical signals. Recent improvements in brain recording and statistical methods have given researchers unprecedented insight into the physical processes under-lying thoughts. For example, researchers have begun to show that it is possible to use brain recordings to reconstruct aspects of an image or movie clip someone is viewing, a sound someone is hearing or even the text someone is reading.

Researchers have long been interested in discovering the ways that human brains represent thoughts through a complex interplay of electrical signals. (Credit: © James Steidl / Fotolia)

A new study by University of Pennsylvania and Thomas Jefferson University scientists brings this work one step closer to actual mind reading by using brain recordings to infer the way people organize associations between words in their memories.

The research was conducted by professor Michael J. Kahana of the Department of Psychology in Penn’s School of Arts and Sciences and graduate student Jere-my R. Manning, then a member of the Neuroscience Graduate Group in Penn’s Perelman School of Medicine. They collaborated with other members of Kahana’s laboratory, as well as with research faculty at Thomas Jefferson University Hospital.

Their study was published in The Journal of Neuroscience.

The brain recordings necessary for the study were made possible by the fact that the participants were epilepsy patients who volunteered for the study while awaiting brain surgery. These participants had tiny electrodes implanted in their brains, which allowed researchers to precisely observe electrical signals that would not have been possible to measure outside the skull. While recording these electrical signals, the researchers asked the participants to study lists of 15 randomly chosen words and, a minute later, to repeat the words back in which-ever order they came to mind.

The researchers examined the brain recordings as the participants studied each word to home in on signals in the participant’ brains that reflected the meanings of the words. About a second before the participants recalled each word, these same “meaning signals” that were identified during the study phase were spontaneously reactivated in the participants’ brains.

Because the participants were not seeing, hearing or speaking any words at the times these patterns were reactivated, the researchers could be sure they were observing the neural signatures of the participants’ self-generated, internal thoughts.

Critically, differences across participants in the way these meaning signals were reactivated predicted the order in which the participants would recall the words. In particular, the degree to which the meaning signals were reactivated before recalling each word reflected each participant’s tendency to group similar words (like “duck” and “goose”) together in their recall sequence. Since the participants were instructed to say the words in the order they came to mind, the specific se-quence of recalls a participant makes provides insights into how the words were organized in that participant’s memory.

In an earlier study, Manning and Kahana used a similar technique to predict participants’ tendencies to organize learned information according to the time in which it was learned. Their new study adds to this research by elucidating the neural signature of organizing learned information by meaning.

"Each person’s brain patterns form a sort of ‘neural fingerprint’ that can be used to read out the ways they organize their memories through associations between words," Manning said.

The techniques the researchers developed in this study could also be adapted to analyze many different ways of mentally organizing studied information.

"In addition to looking at memories organized by time, as in our previous study, or by meaning, as in our current study, one could use our technique to identify neural signatures of how individuals organize learned information according to appearance, size, texture, sound, taste, location or any other measurable property," Manning said.

Such studies would paint a more complete picture of a fundamental aspect of human behavior.

"Spontaneous verbal recall is a form of memory that is both pervasive in our lives and unique to the human species," Kahana said. "Yet, this aspect of human memory is the least well understood in terms of brain mechanisms. Our data show a direct correspondence between patterns of brain activity and the meanings of individual words and show how this neural representation of meaning predicts the way in which one item cues another during spontaneous recall.

"Given the critical role of language in human thought and communication, identifying a neural representation that reflects the meanings of words as they are spontaneously recalled brings us one step closer to the elusive goal of mapping thoughts in the human brain."

Source: Science Daily

ScienceDaily (June 26, 2012) — Rhode Island Hospital researcher Suzanne de la Monte, M.D., has found a link between brain insulin resistance (diabetes) and two other key mediators of neuronal injury that help Alzheimer’s disease (AD) to propagate. The research found that once AD is established, therapeutic efforts must also work to reduce toxin production in the brain.

The study, “Dysfunctional Pro-Ceramide, ER Stress, and Insulin/IGF Signaling Networks with Progression of Alzheimer’s Disease”, is published in the June 22, 2012, supplement of the Journal of Alzheimer’s Disease.

Alzheimer’s disease is one of the most common degenerative dementias, and more than 115 million new cases are projected worldwide in the next 40 years. There is clinical and experimental evidence that treatment with insulin or insulin sensitizer agents can enhance cognitive function and in some circumstances help slow the rate of cognitive decline in AD. Alzheimer’s and other neurodegenerative diseases destroy the brain until the patients finally succumb. In order to effectively halt the process of neurodegeneration, the forces that advance and perpetuate the disease, particularly with regard to the progressive worsening of brain insulin/IGF resistance, must be understood.

"Brain insulin resistance (diabetes) is very much like regular diabetes," de la Monte said. "Since the underlying problems continue to be just about the same, we believe that the development of new therapies would be applicable for all types of diabetes, including Alzheimer’s disease, which we refer to as Type III diabetes."

She continued, “This study points out that once AD is established, therapeutic efforts should target several different pathways — not just one. The reason is that a positive feedback loop gets going, making AD progress. We have to break the vicious cycle. Restoring insulin responsiveness and insulin depletion will help, but we need to reduce brain stress and repair the metabolic problems that cause the brain to produce toxins.”

Ultimately, these findings will help to expand ways to both detect and treat AD.

Growing evidence supports the concept that AD is fundamentally a metabolic syndrome that leads to abnormalities linked to brain insulin and insulin-like growth factor (IGF) resistance. In AD, brain insulin and IGF resistance and deficiencies begin early and worsen with severity of the disease. The rationale behind the progression of the disease is that insulin-resistance dysregulates lipid metabolism and promotes ceramide accumulation, thereby increasing inflammation and lipid metabolism, causing toxic ceramides to accumulate in the brain. The end result is increased stress that threatens the survival and function of neurons in the brain.

The present study was designed to gain a better understanding of how brain insulin resistance becomes progressive and contributes to the neurodegeneration in AD, focusing on the roles of ceramides and stress. The researchers studied the same brain samples used previously to demonstrate progressive impairments in brain insulin/IGF signaling with increasing severity of AD.

Source: Science Daily

June 26, 2012

The inexorable spread of Alzheimer’s disease through the brain leaves dead neurons and forgotten thoughts in its wake. Researchers at Linköping University in Sweden are the first to show how toxic proteins are transferred from neuron to neuron.

Two nerve cells, each about 10 micrometers large, are visible as shadows in this picture. From the beginning only the right one (yellow arrow) contained the toxic, red stained, oligomeric beta-amyloid. When these sick cells make contacts with the healthy, green labeled cells (black arrow), toxic beta-amyloid will spread through the neuronal projections (white arrow). Subsequently, also the green cell will become sick. Credit: Martin Hallbeck

Through experiments on stained neurons, the research team – under the leadership of Martin Hallbeck, associate professor of Pathology – has been able to depict the process of neurons being invaded by diseased proteins that are then passed on to nearby cells.

"The spread of Alzheimer’s, which can be studied in the brains of diseased patients, always follows the same pattern. But until now how and why this happens has not been understood," says Hallbeck, who along with his research group has now published their results in The Journal of Neuroscience.

The illness starts in the entorhinal cortex – a part of the cerebral cortex, and then spreads to the hippocampus. Both of these areas are important for memory. Gradually, pathological changes take place in more and more areas of the brain, while the patient becomes even sicker.

Two proteins have been identified in connection with Alzheimer’s: beta amyloid and tau. Normally tau is found in the axons – the outgrowths that connect between neurons – where it has a stabilising function, while beta amyloid seems to have a role in the synapses where the neurons transfer signal substances to each other. But in Alzheimer’s patients, something happens with these proteins; autopsies reveal abnormal accumulations of both.

Why they become abnormal is still unknown, but what is known is that it’s not the large accumulations, or plaques, that damage the neurons. Instead, smaller groups of beta amyloid – called oligomeres – seem to be the toxic form that gradually destroy the neurons and shrink the brain.

"We wanted to investigate whether these oligomeres can spread from neuron to neuron, something many researchers tried earlier but didn’t succeed," Hallbeck says.

The study was inaugurated with an experiment on neuron cultures, where researchers injected oligomeres stained with a phosphorescent red substance called TMR using a very thin needle. The next day the neighbouring, connected neurons were also red, which showed that the oligomeres had spread.

To test whether a sick neuron can “infect” others, they conducted a round of experiments with mature human neurons stained green and mixed with others that were red after having taken up stained oligomeres. After a day, approximately half of the green cells had been in contact with a few of the red ones. After two more days, the axons had lost their shape and organelles in the cell nucleus had started to leak.

"Gradually more and more of the green cells became sick. Those that hadn’t taken up the oligomeres, on the other hand, weren’t affected," Hallbeck says.

The study is a breakthrough in understanding Alzheimer’s and its progress. If a way of stopping the transfer can be found, it could lead to a more effective inhibitor against the disease.

Provided by Linköping University

Source: medicalxpress.com

June 26, 2012

A new video article in JoVE, the Journal of Visualized Experiments, describes a novel procedure to monitor brain function and aid in functional mapping of patients with diseases such as epilepsy. This procedure illustrates the use of pre-placed electrodes for cortical mapping in the brains of patients who are undergoing surgery to minimize the frequency of seizures. This technique, while invasive, provides real-time analysis of brain function at a much higher resolution than current technologies.

This image shows the implanted electrodes as they are mapped on the brain. Credit: Journal of Visualized Experiments

Typically, functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) are used in neuroimaging studies but these techniques suffer from low temporal and spatial resolution. By using electrodes implanted in the brain of an epileptic patient already undergoing treatment, scientists can now image the brain with a much higher spatial resolution, lower signal interference, and a higher temporal resolution than fMRI or EEG.

The leading author of the study, Dr. Gerwin Schalk, from the New York State Department of Health and Albany Medical College, states, “Essentially, we have created a new imaging technique. Our procedure is innovative because it is prospective, meaning, it can image brain function as it occurs. Further, it does not require an expert to derive meaningful information concerning brain function.” He also notes that it was crucial for this procedure to be demonstrated in a video format. “The procedure is a very visual process. The ancillary information such as the spatial relationships of different components, the set-up of the hospital room, and the set-up of the equipment itself cannot be represented in a typical print article. The video capacities of JoVE were an excellent vehicle to demonstrate both the general set-up and the specific implementation of the mapping system.”

By relying on an epileptic patient’s neural implants, scientists gain an unprecedented insight into the brain’s function. Dr. Schalk’s procedure provides a technological advancement that can be applied in many ways, including stroke patient monitoring and rehabilitation, signal mapping and transduction for movement of prosthetic limbs, and enhancement of communication in individuals with paralysis of the vocal musculature. The JoVE video article provides a comprehensive demonstration of the new technique, from mapping the electrical implants to interpreting the tests in real time. JoVE editor Dr. Claire Standen emphasizes, “The new imaging technique demonstrated in this article is very important. There is a definite need for better, more accurate, imaging to monitor brain function. This technique can be applied to a wide range of clinical areas within the Neuroscience field.” The article can be found here: Recording Human Electrocorticographic (ECoG) Signals for Neuroscientific Research and Real-time Functional Cortical Mapping

Provided by The Journal of Visualized Experiments

Source: medicalxpress.com

June 25, 2012

The same neurological mechanism involved in the transition from habitual to compulsive drug use could underlie less severe, but still harmful, compulsive behaviours.

"We’re trying to understand individuality in addictive behaviour. Many people can be exposed to drugs with addictive potential, for instance, but not everyone will become addicted,” explains Eric Dumont, an associate professor in the Department of Biomedical and Molecular Sciences. “We believe we’ve identified a mechanism that makes certain people predisposed to developing addictions, and it’s possible that the same mechanism underlies many - perhaps most - compulsive behaviours.”

The mechanism occurs in a reward pathway of the brain. In this pathway, the brain maintains a delicate balance between pleasure and aversion, ensuring that moment-to-moment desires and dislikes remain in sync with the biological needs of the body.

Dr. Dumont and his team found unusual activity in this pathway when modeling drug addiction in rats, which exhibit a genetic predisposition to addiction comparable to humans. They believe that the pathway’s balance is prone to becoming unbalanced in a certain percentage of the population. The signal to stop an activity reverses to a green light.

The team hopes that by identifying this mechanism, and possibly others like it, they will allow researchers to better understand and monitor a range of compulsive behaviours. Accordingly, Dr. Dumont’s team collaborates with Dr. Cella Olmstead, associate professor of Psychology at Queen’s, who recently developed an animal model of compulsive sucrose intake.

Dr. Dumont and this team were recently awarded a $520,000 operating grant from Canadian Institutes of Health Research (CIHR) to support their work for the next five years in understanding the neurological processes behind addiction behaviour.

Provided by Queen’s University

Source: medicalxpress.com

ScienceDaily (June 25, 2012) — Deep brain stimulation reduces binge eating in mice, suggesting that this surgery, which is approved for treatment of certain neurologic and psychiatric disorders, may also be an effective therapy for obesity. Presentation of the results took place June 25 at The Endocrine Society’s 94th Annual Meeting in Houston.

"Doing brain surgery for obesity treatment is a controversial idea," said the study’s presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."

Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson’s disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.

Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.

The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.

After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period.

For one week, mice consistently binged, eating almost half of their daily calories during this one hour, the authors reported. Then on alternating days, the investigators turned on the stimulator. On the days that deep brain stimulation was administered, or “on,” the scientists observed a significant (approximately 60 percent) decrease in consumption of the high-fat diet. On the alternate days when they turned off the stimulator, binge eating returned, Halpern said.

The researchers then studied how deep brain stimulation might work to improve binge eating. With medications, they blocked various receptors of dopamine neurons, or nerve cells. Dopamine is a brain neurotransmitter, a chemical messenger, whose release in the brain is linked to the desire for rewarding behaviors such as eating high-fat food, according to Halpern.

Only one of the medications had an effect. Raclopride, which blocks the type 2 dopamine receptor, weakened the beneficial effect of deep brain stimulation by 50 percent.

Their results, Halpern said, showed that “at least one way that deep brain stimulation functions to suppress binge eating might be by modulating activity of neurons expressing the type 2 dopamine receptor.”

Source: Science Daily

June 25, 2012 By Rick Nauert

A new study involving children with Williams syndrome (WS) suggests that improved regulation of oxytocin and vasopressin may someday improve care for autism, anxiety, post-traumatic stress disorder and WS.

WS results when certain genes are absent because of a faulty recombination event during the development of sperm or egg cells. Virtually everyone with WS has exactly the same set of genes missing (25 to 28 genes are missing from one of two copies of chromosome 7).

“The genetic deficiencies allow researchers to examine the genetic and neuronal basis of social behavior,” said Ursula Bellugi, Ph.D., a co-author on the paper.

“This study provides us with crucial information about genes and brain regions involved in the control of oxytocin and vasopressin, hormones that may play important roles in other disorders.”

In the study, scientists at the Salk Institute for Biological Studies and the University of Utah, found that people with WS flushed with the hormones oxytocin and arginine vasopressin (AVP) when exposed to emotional triggers.

Children with WS love people, despite being challenged with numerous health problems. WS kids are extremely gregarious, irresistibly drawn to strangers, and insist on making eye contact.

They have an affinity for music. But they also experience heightened anxiety, have an average IQ of 60, experience severe spatial-visual problems, and suffer from cardiovascular and other health issues.

Yet despite their desire to befriend people, WS kids have difficulty creating and maintaining social relationships — an issue that obviously affects many people without WS.

In the new study, led by Julie R. Korenberg, M.D., 21 participants, 13 who have WS and a control group of eight people without the disorder were evaluated at the Cedars-Sinai Medical Center in Los Angeles. Because music is a known strong emotional stimulus, the researchers asked participants to listen to music.

Before the music was played, the participants’ blood was drawn to determine a baseline level for oxytocin. Remarkably, those with WS had three times as much of the hormone as those without the syndrome.

Blood also was drawn at regular intervals while the music played and was analyzed afterward to check for real-time, rapid changes in the levels of oxytocin and AVP.

While other studies have examined how oxytocin affects emotion when artificially introduced into people, such as through nasal sprays, this is one of the first significant studies to measure naturally occurring changes in oxytocin levels in rapid, real time as people undergo an emotional response.

Although the WS participants displayed little outward response to the music, an analyses of blood samples showed that the oxytocin levels, and to a lesser degree AVP, had increased sharply while they had listened to the music.

In contrast, among those without WS, both the oxytocin and AVP levels remained largely unchanged as they listened to music.

Korenberg believes the blood analyses strongly indicate that oxytocin and AVP are not regulated correctly in people with WS, and that the behavioral characteristics unique to people with WS are related to this problem. “This shows that oxytocin quite likely is very involved in emotional response,” she said.

In addition to listening to music, study participants already had taken three social behavior tests that evaluate willingness to approach and speak to strangers, emotional states, and various areas of adaptive and problem behavior.

Those test results suggest that increased levels of oxytocin are linked to both increased desire to seek social interaction and decreased ability to process social cues, a double-edged message that may be very useful at times, for example, during courtship, but damaging at others, as in WS.

“The association between abnormal levels of oxytocin and AVP and altered social behaviors found in people with Williams Syndrome points to surprising, entirely unsuspected deleted genes involved in regulation of these hormones and human sociability,” Korenberg said.

“It also suggests that the simple characterization of oxytocin as ‘the love hormone’ may be an overreach. The data paint a far more complicated picture.”

Overall, the researchers say, their findings paint a hopeful picture, and the study holds promise for speeding progress in treating WS, and perhaps autism and anxiety through regulation of these key players in human brain and emotion, oxytocin and vasopressin.

Source: PsychCentral

ScienceDaily (June 25, 2012) — Researchers have discovered how a hormone in the gut slows the rate at which the stomach empties and thus suppresses hunger and food intake. Results of the animal study were presented June 25 at The Endocrine Society’s 94th Annual Meeting in Houston.

"The gut hormone glucagon-like peptide 2, or GLP-2, functions as a neurotransmitter and fine-tunes gastric emptying through — as suspected — its receptor action in the brain," said the lead investigator, Xinfu Guan, PhD, assistant professor of pediatrics and medicine at Baylor College of Medicine in Houston.

The researchers found that this action occurs in the GLP-2 receptor specifically in a key group of nerve cells in the brain, called pro-opiomelanocortin, or POMC, neurons. These neurons are in the hypothalamus, the part of the brain that produces appetite-controlling neuropeptides.

In their study using molecular methods, mice lacking this GLP-2 receptor in the POMC neurons showed late-onset obesity and higher food intake compared with normal wild-type mice. The mutant, or GLP-2 receptor “knockout,” mice also had accelerated gastric emptying after a liquid meal, as found on a noninvasive breath test. The faster the gastric emptying, the higher the food intake, scientists know.

Therefore, obese people may have something wrong with this hormone receptor, which alters their gastric emptying rate, Guan speculated. Many studies have shown that nondiabetic, obese humans have accelerated gastric emptying.

The researchers also found that this receptor quickly activated the PI3K intracellular signaling pathway in the POMC neurons. This, in turn, induces neuronal excitation (transmission of signals) and gene expression, according to Guan.

These findings, Guan said, show that in the central nervous system the GLP-2 receptor plays an important physiological role in the control of food intake and gastric emptying.

"This study has advanced our understanding of the brain-gut neural circuits that mediate eating behavior via modulating gastric emptying, which contributes to the control of body weight," he said.

Source: Science Daily