Sensory Neurons Identified as Critical to Sense of Touch
While studying the sense of touch, scientists at Duke Medicine have pinpointed specific neurons that appear to regulate perception. The sensory neurons are characterized by thin spikes, and based on their volume, these protrusions determine the cells’ sensitivity to force.
The findings in fruit fly larvae, which appear in online Oct. 25, 2012, in the journal Current Biology, demonstrate the first known function for the sensory neurons and provide insights that could broaden the understanding of chronic pain syndromes in humans.
"On a molecular level, touch is the most poorly understood of the senses," said W. Daniel Tracey, PhD, associate professor of anesthesiology at Duke University Medical Center and study author. "While there are many types of touch sensor neurons, we still don’t know how these neurons respond to force."
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Researchers from UCL have found that lonely people have less grey matter in a part of the brain associated with decoding eye gaze and other social cues.
Published in the journal of Current Biology, the study also suggests that through training people might be able to improve their social perception and become less lonely.
“What we’ve found is the neurobiological basis for loneliness,” said lead author Dr Ryota Kanai (UCL Institute of Cognitive Neuroscience). “Before conducting the research we might have expected to find a link between lonely people and the part of the brain related to emotions and anxiety, but instead we found a link between loneliness and the amount of grey matter in the part of the brain involved in basic social perception.”
To see how differences in loneliness might be reflected in the structure of the brain regions associated with social processes, the team scanned the brains of 108 healthy adults and gave them a number of different tests. Loneliness was self-reported and measured using a UCLA loneliness scale questionnaire.
When looking at full brain scans they saw that lonely individuals have less greymatter in the left posterior superior temporal sulcus (pSTS)—an area implicated in basic social perception, confirming that loneliness was associated with difficulty in processing social cues.
“The pSTS plays a really important role in social perception, as it’s the initial step of understanding other people,” said Dr Kanai. “Therefore the fact that lonely people have less grey matter in their pSTS is likely to be the reason why they have poorer perception skills.”
In order to gauge social perception, participants were presented with three different faces on a screen and asked to judge which face had misaligned eyes and whether they were looking either right or left. Lonely people found it much harder to identify which way the eyes were looking, confirming the link between loneliness, the size of the pSTS and the perception of eye gaze.
“From the study we can’t tell if loneliness is something hardwired or environmental,” said co-author Dr Bahador Bahrami (UCL Institute of Cognitive Neuroscience). “But one possibility is that people who are poor at reading social cues may experience difficulty in developing social relationships, leading to social isolation and loneliness.”
One way to counter this loneliness could be through social perception training with a smartphone app.
“The idea of training is one way to address this issue, as by maybe using a smartphone app to improve people’s basic social perception such as eye gaze, hopefully we can help them to lead less lonely lives,” said Dr Kanai.
(Source: ucl.ac.uk)
Filed under brain social perception loneliness emotion eye gaze neuroscience psychology science
3D fetus fly-through peers inside abnormal bodies
Thanks to MRI techniques, you can see what a baby looks like before it’s born. But now these images can also be used to peer inside the body of a fetus, generating a fly-through of internal tissues that rivals the view you would get from a video.
Developed by Jorge Lopes from the National Institute of Technology (INT) in Rio de Janeiro, Brazil, and colleagues, the system can quickly produce a 3D virtual tour through a region of interest, usually to examine congenital anomalies. Using a combination of software, a doctor can produce a reconstruction after an MRI scan by selecting the camera angle and movement desired. In this video, a view into the lungs and airways of two unborn babies with tumours helped determine if their breathing would be affected after birth.
In addition to virtual models, the team can also produce 3D printed versions of an unborn child (see image above). According to Lopes, physical models can help describe a condition to expectant parents and illustrate surgical procedures required, as well as being useful for blind mothers to get a sense of their baby’s appearance.
Filed under fetus development MRI virtual tour congenital anomalies tumors science

Joint research between the University of Michigan and the Argentina-based National Council of Science and Technology (CONICET) has shed light on one of the most frustrating mysteries of weight loss – why the weight inevitably comes back.
A novel animal model showed that the longer mice remained overweight, the more “irreversible” obesity became, according to the new study that appeared online ahead of print Oct.24 in the Journal of Clinical Investigation.
Over time, the static, obese state of the mice reset the “normal,” body weight set point to become permanently elevated, despite dieting that initially worked to shed pounds, authors say.
“Our model demonstrates that obesity is in part a self-perpetuating disorder and the results further emphasize the importance of early intervention in childhood to try to prevent the condition whose effects can last a lifetime,” says senior author Malcolm J. Low, M.D., Ph.D., professor of molecular and integrative physiology and internal medicine.
(Source: uofmhealth.org)
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Study finds moderate consumption decreases number of new brain cells

Drinking a couple of glasses of wine each day has generally been considered a good way to promote cardiovascular and brain health. But a new Rutgers University study indicates that there is a fine line between moderate and binge drinking – a risky behavior that can decrease the making of adult brain cells by as much as 40 percent.
In a study posted online and scheduled to be published in the journal Neuroscience on November 8, lead author Megan Anderson, a graduate student working with Tracey J. Shors, Professor II in Behavioral and Systems Neuroscience in the Department of Psychology, reported that moderate to binge drinking – drinking less during the week and more on the weekends – significantly reduces the structural integrity of the adult brain.
“Moderate drinking can become binge drinking without the person realizing it,” said Anderson.“In the short term there may not be any noticeable motor skills or overall functioning problems, but in the long term this type of behavior could have an adverse effect on learning and memory.”
(Source: news.rutgers.edu)
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In an early-stage breakthrough, a team of Northwestern University scientists has developed a new family of compounds that could slow the progression of Parkinson’s disease.
Parkinson’s, the second most common neurodegenerative disease, is caused by the death of dopamine neurons, resulting in tremors, rigidity and difficulty moving. Current treatments target the symptoms but do not slow the progression of the disease.
The new compounds were developed by Richard B. Silverman, the John Evans Professor of Chemistry at the Weinberg College of Arts and Sciences and inventor of the molecule that became the well-known drug Lyrica, and D. James Surmeier, chair of physiology at Northwestern University Feinberg School of Medicine. Their research was published Oct. 23 in the journal Nature Communications.
The compounds work by slamming the door on an unwelcome and destructive guest — calcium. The compounds target and shut a relatively rare membrane protein that allows calcium to flood into dopamine neurons. Surmeier’s previously published research showed that calcium entry through this protein stresses dopamine neurons, potentially leading to premature aging and death. He also identified the precise protein involved — the Cav1.3 channel.
"These are the first compounds to selectively target this channel," Surmeier said. "By shutting down the channel, we should be able to slow the progression of the disease or significantly reduce the risk that anyone would get Parkinson’s disease if they take this drug early enough."
"We’ve developed a molecule that could be an entirely new mechanism for arresting Parkinson’s disease, rather than just treating the symptoms," Silverman said.
The compounds work in a similar way to the drug isradipine, for which a Phase 2 national clinical trial with Parkinson’s patients –- led by Northwestern Medicine neurologist Tanya Simuni, M.D. — was recently completed. But because isradipine interacts with other channels found in the walls of blood vessels, it can’t be used in a high enough concentration to be highly effective for Parkinson’s disease. (Simuni is the Arthur C. Nielsen Professor of Neurology at the Feinberg School and a physician at Northwestern Memorial Hospital.)
The challenge for Silverman was to design new compounds that specifically target this rare Cav1.3 channel, not those that are abundant in blood vessels. He and colleagues first used high-throughput screening to test 60,000 existing compounds, but none did the trick.
"We didn’t want to give up," Silverman said. He then tested some compounds he had developed in his lab for other neurodegenerative diseases. After Silverman identified one that had promise, Soosung Kang, a postdoctoral associate in Silverman’s lab, spent nine months refining the molecules until they were effective at shutting only the Cav1.3 channel.
In Surmeier’s lab, the drug developed by Silverman and Kang was tested by graduate student Gary Cooper in regions of a mouse brain that contained dopamine neurons. The drug did precisely what it was designed to do, without any obvious side effects.
"The drug relieved the stress on the cells," Surmeier said.
For the next step, the Northwestern team has to improve the pharmacology of the compounds to make them suitable for human use, test them on animals and move to a Phase 1 clinical trial.
"We have a long way to go before we are ready to give this drug, or a reasonable facsimile, to humans, but we are very encouraged," Surmeier said.
(Source: eurekalert.org)
Filed under brain neurodegenerative diseases parkinson parkinson's disease neuroscience science
Challenging Parkinson’s Dogma: Dopamine may not be the only key player in this tragic neurodegenerative disease
Scientists may have discovered why the standard treatment for Parkinson’s disease is often effective for only a limited period of time. Their research could lead to a better understanding of many brain disorders, from drug addiction to depression, that share certain signaling molecules involved in modulating brain activity.
A team led by Bernardo Sabatini, Takeda Professor of Neurobiology at Harvard Medical School, used mouse models to study dopamine neurons in the striatum, a region of the brain involved in both movement and learning. In people, these neurons release dopamine, a neurotransmitter that allows us to walk, speak and even type on a keyboard. When those cells die, as they do in Parkinson’s patients, so does the ability to easily initiate movement. Current Parkinson’s drugs are precursors of dopamine that are then converted into dopamine by cells in the brain.
The flip side of dopamine dearth is dopamine hyperactivity. Heroin, cocaine and amphetamines rev up or mimic dopamine neurons, ultimately reinforcing the learned reward of drug-taking. Other conditions such as obsessive-compulsive disorder, Tourette syndrome and even schizophrenia may also be related to the misregulation of dopamine.
In the October 11 issue of Nature, Sabatini and co-authors Nicolas Tritsch and Jun Ding reported that midbrain dopamine neurons release not only dopamine but also another neurotransmitter called GABA, which lowers neuronal activity. The previously unsuspected presence of GABA could explain why restoring only dopamine could cause initial improvements in Parkinson’s patients to eventually wane. And if GABA is made by the same cells that produce other neurotransmitters, such as depression-linked serotonin, similar single-focus treatments could be less successful for the same reason.
“If what we found in the mouse applies to the human, then dopamine’s only half the story,” said Sabatini.
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Researchers Identify Area of the Brain That Processes Empathy
An international team led by researchers at Mount Sinai School of Medicine in New York has for the first time shown that one area of the brain, called the anterior insular cortex, is the activity center of human empathy, whereas other areas of the brain are not. The study is published in the September 2012 issue of the journal Brain.
Empathy, the ability to perceive and share another person’s emotional state, has been described by philosophers and psychologists for centuries. In the past decade, however, scientists have used powerful functional MRI imaging to identify several regions in the brain that are associated with empathy for pain. This most recent study, however, firmly establishes that the anterior insular cortex is where the feeling of empathy originates.
“Now that we know the specific brain mechanisms associated with empathy, we can translate these findings into disease categories and learn why these empathic responses are deficient in neuropsychiatric illnesses, such as autism,” said Patrick R. Hof, MD, Regenstreif Professor and Vice-Chair, Department of Neuroscience at Mount Sinai, a co-author of the study. “This will help direct neuropathologic investigations aiming to define the specific abnormalities in identifiable neuronal circuits in these conditions, bringing us one step closer to developing better models and eventually preventive or protective strategies.”
Filed under brain anterior insular cortex empathy emotion perception neuroscience psychology science
“Grassroots” Neurons Wire and Fire Together for Dominance in the Brain
Inside the brain, an unpredictable race—like a political campaign—is being run. Multiple candidates, each with a network of supporters, have organized themselves into various left- and right-wing clusters—like grassroots political teams working feverishly to reinforce a vision that bands them together. While scientists know that neurons in the brain anatomically organize themselves into these network camps, or clusters, the implications of such groupings on neural dynamics have remained unclear until now.
Using mathematical modeling, two researchers from the University of Pittsburgh have found that neurons team up together to sway particular outcomes in the brain and take over the nervous system in the name of their preferred action or behavior. The findings will be published in the November print issue of Nature Neuroscience.
“Through complex mathematical equations, we organized neurons into clustered networks and immediately saw that our model produced a rich dynamic wherein neurons in the same groups were active together,” said Brent Doiron, assistant professor of mathematics.
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Brainwave Training Boosts Network for Cognitive Control and Predicts Mind Wandering
A breakthrough study conducted in Canada has found that training of the well-known brainwave in humans, the alpha rhythm, enhances a brain network responsible for cognitive-control which correlates with reductions in mind-wandering. The training technique, termed neurofeedback, is being considered as a promising method for restoring brain function in mental disorders. Using several neuroimaging methods, a team of researchers working at the University of Western Ontario have now uncovered that functional changes within a key brain network occur directly after a 30-minute session of noninvasive, neural-based training. Dysfunction of this cognitive-control network has previously been implicated in a range of brain disorders including attentional deficit hyperactivity disorder, schizophrenia, depression and post-traumatic stress disorder.
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