Chapter 16. None
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Susan Milius Electric eels are even more shocking than biologists thought. When prey fights back, eels just — curl their tails. Muscle has evolved “into a battery” independently in two groups of fishes, explains Kenneth Catania of Vanderbilt University in Nashville. Smaller species send out slight tingles of electric current that detect the fish’s surroundings in murky nighttime water. People can handle these small fishes and not feel even a tickle. But touching the bigger Electrophorus electricus (a member of a South American group of battery-included fishes)“is reminiscent of walking into an electric fence on a farm,” Catania says. (He knows, unintentionally, from experience.) The modified muscle that works as an electricity-generating organ in the eel has just on/off power. But eels have a unique way of intensifying the effect, Catania reports October 28 in Current Biology. Catania has tussled with eels using what he calls his electric eel chew toy — a dead fish on a stick with electrodes inside the carcass to measure current. When fighting difficult prey Iike the recalcitrant toy, eels curl their tails toward the fish struggling in their jaws. This bend puts the electrically negative tail-end of the long battery organ closer to the electrically positive front end, effectively concentrating the electric field on the prey. An eel’s tail curl can double the strength of the electric field convulsing the prey. © Society for Science & the Public 2000 - 2015.
By Nicholas Bakalar Certain personality traits are often attributed to oldest, middle and youngest children. But a new study found that birth order itself had no effect on character, though it may slightly affect intelligence. Researchers analyzed three large ongoing collections of data including more than 20,000 people: a British study that follows the lives of people who were born in one particular week in 1958, a German study of private households started in 1984 and a continuing study of Americans born between 1980 and 1984. They searched for differences in extroversion, emotional stability, agreeableness, conscientiousness, self-reported intellect, IQ, imagination and openness to experience. They analyzed families with sisters and brothers, large and small age gaps and different numbers of siblings. They even looked to see if being a middle child correlated with any particular trait. But no matter how they spliced the data, they could find no association of birth order with any personality characteristic. The study, in Proceedings of the National Academy of Sciences, did find evidence that older children have a slight advantage in IQ scores, but the difference was apparent only in a large sample, with little significance for any individual. The lead author, Julia M. Rohrer, a graduate student at the University of Leipzig, said that birth order can have an effect — if your older brother bullied you, for example. “But these effects are highly idiosyncratic,” she said. “There is no such thing as a typical older, middle or younger sibling. It’s important to stop believing that you are the way you are because of birth order.” © 2015 The New York Times Company
A drug for Alzheimer’s seems to delay the point at which a person with the condition needs to be moved into a nursing home. Donepezil is usually given to people with moderate forms of the disease, but continuing to take the drug once the disease becomes more severe seems to prolong the period of time a person can remain in their own home. Previously, the drug was not thought to benefit people once they had developed more severe forms of Alzheimer’s. But a study that followed 295 people with moderate to severe Alzheimer’s disease found that those who continued to take donepezil were nearly half as likely to end up in a care home within the next year. “It could mean thousands of patients per year not going into care homes,” says Robert Howard of University College London, who led the study. His team found that those who continued to take donepezil had a 20 per cent chance of being moved into a care home within the first year of the trial, compared to 37 per cent in those who stopped taking the drug. However the effect didn’t last. The trial lasted for three years, and after the first year, those who taking donepezil were just as likely to be moved into a home than those who weren’t, suggesting that the drug does not have a longer-term effect on the care needs of those with Alzheimer’s. “For every six patients treated with donepezil for 12 months, you would prevent one moving into a nursing home,” says Howard. “It’s a modest effect, but it’s important if it’s your mother or your wife.” © Copyright Reed Business Information Ltd.
Link ID: 21577 - Posted: 10.28.2015
Looking at brain tissue from mice, monkeys and humans, scientists have found that a molecule known as growth and differentiation factor 10 (GDF10) is a key player in repair mechanisms following stroke. The findings suggest that GDF10 may be a potential therapy for recovery after stroke. The study, published in Nature Neuroscience, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “These findings help to elucidate the mechanisms of repair following stroke. Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery,” said Francesca Bosetti, Ph.D., stroke program director at NINDS. Stroke can occur when a brain blood vessel becomes blocked, preventing nearby tissue from getting essential nutrients. When brain tissue is deprived of oxygen and nutrients, it begins to die. Once this occurs, repair mechanisms, such as axonal sprouting, are activated as the brain attempts to overcome the damage. During axonal sprouting, healthy neurons send out new projections (“sprouts”) that re-establish some of the connections lost or damaged during the stroke and form new ones, resulting in partial recovery. Before this study, it was unknown what triggered axonal sprouting. Previous studies suggested that GDF10 was involved in the early stages of axonal sprouting, but its exact role in the process was unclear. S. Thomas Carmichael, M.D., Ph.D., and his colleagues at the David Geffen School of Medicine at the University of California Los Angeles took a closer look at GDF10 to identify how it may contribute to axonal sprouting.
by Helen Thompson Five, six, seven, eight! All together now, let's spread those jazz hands and get moving, because synchronized dancing improves our tolerance of pain and helps us bond as humans, researchers suggest October 28 in Biology Letters. A team of psychologists at the University of Oxford taught high school students varied dance routines — each requiring different levels of exertion and synchronized movement — and then tested their pain tolerance with the sharp squeeze of a blood pressure cuff. Statistically, routines with more coordinated choreography and full body movement produced higher pain thresholds and sunny attitudes toward others in the group. Coordinated dancing with a group and exerting more energy may independently promote the release of pain-blocking endorphins as well as increase social bonding, the team writes. |© Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21575 - Posted: 10.28.2015
By GINA KOLATA Three diseases, leading killers of Americans, often involve long periods of decline before death. Two of them — heart disease and cancer — usually require expensive drugs, surgeries and hospitalizations. The third, dementia, has no effective treatments to slow its course. So when a group of researchers asked which of these diseases involved the greatest health care costs in the last five years of life, the answer they found might seem surprising. The most expensive, by far, was dementia. The study looked at patients on Medicare. The average total cost of care for a person with dementia over those five years was $287,038. For a patient who died of heart disease it was $175,136. For a cancer patient it was $173,383. Medicare paid almost the same amount for patients with each of those diseases — close to $100,000 — but dementia patients had many more expenses that were not covered. On average, the out-of-pocket cost for a patient with dementia was $61,522 — more than 80 percent higher than the cost for someone with heart disease or cancer. The reason is that dementia patients need caregivers to watch them, help with basic activities like eating, dressing and bathing, and provide constant supervision to make sure they do not wander off or harm themselves. None of those costs were covered by Medicare. For many families, the cost of caring for a dementia patient often “consumed almost their entire household wealth,” said Dr. Amy S. Kelley, a geriatrician at Icahn School of Medicine at Mt. Sinai in New York and the lead author of the paper published on Monday in the Annals of Internal Medicine. © 2015 The New York Times Company
Link ID: 21571 - Posted: 10.27.2015
By Dina Fine Maron When powerful street drugs collectively known as synthetic pot are smoked, the resulting high mimics the effects of marijuana. Yet these man-made cannabinoids are not marijuana at all. The drugs, more commonly called spice, fake weed or K2, are made up of any number of dried, shredded plants sprayed with chemicals that live in a murky legality zone. They are highly dangerous—and their use is on the rise. Synthetic pot, which first hit the market in the early 2000s, has especially caught the attention of public health officials in the past couple of years, stemming from a surge in hospitalizations and violent episodes. Although the drugs act on the same brain pathway as weed's active ingredient, they can trigger harsher reactions, including heart attacks, strokes, kidney damage and delusions. Between June and early August usage of these drugs led to roughly 2,300 emergency room visits in New York State alone. Nationwide more than 6,000 incidents involving spice have been reported to U.S. poison-control centers this year—about double the number of calls in 2013. Ever changing recipes make it possible for spice sellers to elude the authorities. Each time an ingredient is banned, producers swap in another compound. The drugs are then sold on the Internet or at gas stations and convenience stores at prices lower than genuine marijuana. The changing formulations also pose a challenge for researchers trying to match the chemicals with their side effects or to develop tests to identify them in a user's system. “The drugs are present in blood for only a short period, so it's very difficult to detect them,” says Marilyn Huestis, chief of the Chemistry and Drug Metabolism Section at the National Institute on Drug Abuse. © 2015 Scientific American
Keyword: Drug Abuse
Link ID: 21570 - Posted: 10.27.2015
Dyscalculia is like dyslexia — but for those who have trouble with math instead of reading. But not enough people know about it, according to a neuroscientist. "There is a lack of awareness among teachers and educators," said Daniel Ansari, professor and Canada Research Chair in Developmental Cognitive Neuroscience at the University of Western Ontario. Individuals with dyscalculia have trouble with simple calculations. "If I ask you what is 1 + 3, you don't need to calculate. Four will pop in to your head, it is stored in your long-term memory," he said. But those with dyscalculia will have to use their hands to count. Scientists have known about dyscalculia since the 1940's but little research has been done on it, even though it is probably just as common as dyslexia, says Ansari. Currently, there is no existing universal form of testing for dyscalculia. But Ansari has come up with screening tests for children in kindergarten. He says it's important to diagnose dyscalculia early on, so individuals can learn to adapt and improve their skills before it's too late. "We don't just need math to be good in school but to function in society," said Ansari. He says research has shown poor math skills can lead to an increased chance of unemployment, imprisonment or mortgage default. ©2015 CBC/Radio-Canada.
Link ID: 21564 - Posted: 10.26.2015
By Nicholas Bakalar A new study has found that sleep apnea is associated with an increased risk for gout, a painful disease of the big toe and other joints caused by elevated levels of uric acid in the blood. Observational studies have shown that people with sleep apnea have a higher prevalence of excess uric acid, but until now it has been unclear whether sleep apnea is associated with gout, and how strongly. Using records in a British health database, researchers studied 9,865 people, average age 54, with sleep apnea and matched them to 43,598 controls without the disorder. Because sleep apnea is associated with being overweight, the participants were matched for B.M.I., among many other characteristics. The study is in Arthritis & Rheumatology. After one year, compared with controls, people with sleep apnea were about 50 percent more likely to have had an attack of gout, and the increased risk was found without regard to sex, age or obesity. The conclusion suggests that treating sleep apnea would reduce gout attacks, but the lead author, Yuqing Zhang, a professor of medicine at Boston University, is cautious. “Our findings call for future studies to evaluate the effect of treating sleep apnea on serum uric acid levels and the risk of gout,” he said. © 2015 The New York Times Company
Link ID: 21563 - Posted: 10.26.2015
As we get older, most of us will experience some kind of brain degeneration. Typically, we lose the ability to make new neurons. Another problem is chronic, low-grade inflammation in the brain, which is implicated in many age-related brain disorders. To tackle both problems in one go, Ludwig Aigner at Paracelsus Medical University Salzburg in Austria and his colleagues targeted a set of receptors in the brain that, when activated, trigger inflammation. High numbers of these receptors are found in areas of the brain where neurons are born, suggesting they might also be involved in this process, too. A drug called montelukast (Singulair), regularly prescribed for asthma and allergic rhinitis, blocks these receptors, so Aigner and his colleagues tried it on young and old rats. The team used oral doses equivalent to those taken by people with asthma. The older animals were 20 months old – roughly equivalent to between 65 and 75 in human years. The younger rats were 4 months old – about 17 in human years. The animals were fed the drug daily for six weeks, while another set of young and old rats were left untreated. There were 20 young and 14 old rats in total. The rats took part in a range of learning and memory tests. One of these, for example, involved the rats being placed in a pool of water with a hidden escape platform. At the start of the study, untreated young rats learned to recognise landmarks and quickly find their way to the platform, while the untreated older animals struggled at the task. © Copyright Reed Business Information Ltd.
By R. Douglas Fields “Why can’t you stop drinking?” This week at the Annual Meeting of the Society for Neuroscience in Chicago, researchers from the University of Chicago announced a new finding that provides a fresh answer to this persistent question that plagues people addicted to alcohol. The discovery offers an entirely new approach to treatment. Neuroscientist, Amy Lasek, at the Department of Psychiatry at the University of Illinois, Chicago, and colleagues, report that after binge drinking, neurons in brain circuits responsible for alcohol addiction become encased in a protein material, called a perineuronal net. The impenetrable coating cements neurons involved in alcohol addiction into a circuit that is extremely difficult to break. Current drugs for treating alcohol dependence work by modifying neurotransmitter signaling between neurons, but for many people these treatments cannot break the overwhelming compulsion to drink. Drugs that can break down the glue-like cement in perineuronal nets could offer a new approach to treatment. Lasek’s unusual approach into addiction research stems from her background as a molecular and cell biologist working in the field of cancer research. The root of cancer is changes in specific genes. Small molecules designed to target these aberrant genes is the approach used in cancer therapy. Lasek’s background made her think of finding molecularly targeted therapies for psychiatric disorders. Lasek and her colleagues began by studying fruit flies to search for gene variations that altered the fly’s behavior toward alcohol. She found several genes that had this effect, including an obscure one called ALK (anaplastic lymphoma kinase). Then she suppressed these genes in mice to see if the animal’s response to alcohol was altered. “I got hooked,” she says, “because to me the fact that you can manipulate a single gene in a single brain region and change behavior—like drinking or cocaine reward—was fascinating from a biological point of view!” © 2015 Scientific America
Keyword: Drug Abuse
Link ID: 21561 - Posted: 10.24.2015
By Carrie Arnold Most of the anorexia patients Dr. Joanna Steinglass sees in the inpatient eating-disorders unit at the New York State Psychiatric Institute have been to treatment before. While in the hospital or a residential treatment center, they generally gained weight and began to eat a wider variety of foods. But after they left, their old anorexic habits returned. They began skipping meals again or returning to their extreme exercise routines. All too soon, it seemed, the gains made in treatment and the hope for recovery that went along with it began to evaporate. According to the conventional wisdom around eating disorders, these relapses were really a misguided search for control. Or maybe the patients just weren’t ready for recovery yet. Or perhaps these were signs of self-control gone awry, spurred on by friends who marvel at their seemingly endless willpower. Interesting theories, and yet Steinglass disagreed. “Even when people show up at our hospital and want to make changes, they find it tough,” she said. Now a new study in Nature Neuroscience — which Steinglass co-authored — reveals why people with anorexia often struggle so much to integrate new ways of eating into their lives. In the brain, the behaviors associated with anorexia act a lot like habits, those daily decisions we make without thinking. And habits, according to both the scientific evidence and the colloquial wisdom, are phenomenally difficult to break. This new finding helps explain why anorexia has historically been so hard to treat: Anorexic patients are essentially fighting their own brains in an uphill battle for wellness. But more important, the new research may also point toward new and better ways to help those with the eating disorder overcome it. © 2015, New York Media LLC.
Keyword: Anorexia & Bulimia
Link ID: 21560 - Posted: 10.24.2015
Elizabeth Blair The muppet Julia has not yet made her TV debut, but the wide-eyed little girl with a big smile is the star of her own "digital storybook" called "We're Amazing, 1,2,3." For over a year now, Sesame Street has been working with organizations such as Autism Speaks and Autism Self Advocacy to help reduce the stigma associated with autism spectrum disorder. As part of the campaign "See Amazing in All Children," the adorable muppet Abby Cadabby explains in one YouTube video, "Lots of kids have autism and that just means their brains work a little differently." Julia is not the first fictional media character with autism. But Michael Robb, Director of Research for Common Sense Media, an organization that rates and reviews media aimed at children, says Sesame Street's move is "pretty groundbreaking." "It can be difficult to start a conversation about children with disabilities. It's even harder when that difference isn't visible," he says. After looking through "We're Amazing, 1,2,3," Robb says the story could help children be more understanding of how Julia is different. "It's very real in terms of talking in simple language. It spells out these things in concrete ways that kids can understand. It shows ways she's just like other kids. It shows how making simple accommodations can help Julia." According to Dr. Jeanette Betancourt, Senior Vice President of U.S. Social Impact at Sesame Workshop, says Sesame Street producers are waiting to hear back from the autism community before introducing Julia to the show on TV. © 2015 npr
Link ID: 21557 - Posted: 10.24.2015
Olivia Maynard It has been described as a ‘disruptive technology’ potentially capable of breaking our fatal relationship with tobacco. So the setting for a public debate on e-cigarettes - a museum part-funded by the tobacco industry, in a city home to the global headquarters of one of the largest tobacco manufacturers - was perhaps ironic. Yet on Wednesday evening, I found myself at the M-Shed in Bristol, watching just that: a debate about whether e-cigarettes could be part of the solution to the tobacco epidemic. To mark the launch of a new Integrative Cancer Epidemiology Programme, linked to the Medical Research Centre Integrative Epidemiology Unit at the University of Bristol, Professor Marcus Munafò (Professor of Biological Psychology at the University of Bristol) and Professor Linda Bauld (Professor of Health Policy at the University of Stirling), both collaborators of mine, discussed e-cigarettes. Professor Gabriel Scally (Public Health Doctor and former Regional Director of Public Health for the South West of England) chaired the discussion. Billed as a debate about whether e-cigarettes might be ‘the key to reducing smoking’, some in the audience may have expected a heated discussion. However, with this line-up of academics, influential in the fields of public health, tobacco and addiction, the discussion was evidence-based and measured. As for the motion of the debate, the panel was unanimous: e-cigarettes may not be the key to reducing smoking, but they are certainly an important part of the solution. © 2015 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 21556 - Posted: 10.24.2015
Jon Hamilton For a few days this week, a convention center in Chicago became the global epicenter of brain science. Nearly 30,000 scientists swarmed through the vast hallways of the McCormick Place convention center as part of the annual Society for Neuroscience meeting. Among them were Nobel Prize winners, the director of the National Institutes of Health, and scores of researchers regarded as the international rock stars of neuroscience. "It's amazing. I'm a bit overwhelmed," said Kara Furman, a graduate student from Yale who was attending her first Society for Neuroscience meeting. Furman was just one of several hundred neuroscientists I found standing in lines outside the center one afternoon, waiting for shuttle buses. She was pondering a presentation from a few hours earlier that she found "pretty mind-blowing." What was it about? "Using MRI techniques to access dopamine release at the molecular level," she told me, deadpan. Welcome to the five-day annual event that's become known simply as "The Neuro Meeting." It's where brain scientists from around the world come to present their own work and discover the "mind-blowing" research others are doing. And there are thousands of presentations to choose from. "I prepared an itinerary based on my interests and that ran into 20 pages," said Srinivas Bharath from the National Institute of Mental Health and Neurosciences in Bangalore, India. © 2015 npr
Link ID: 21553 - Posted: 10.23.2015
By Melissa Dahl Next time you feel you are in danger of losing an argument, make some obscure reference to the brain. Any nod to neuroscience will do, even if it doesn’t actually illuminate the problem at hand or prove anything that halfway resembles a point. People tend to find explanations that include references to the brain very convincing, even if those references are mostly nonsense, according to the latest episode of "Psych Crunch," a podcast hosted by psychologist (and Science of Us contributor) Christian Jarrett. Jarrett interviews Sara Hodges, a research psychologist at the University of Oregon and the co-author of a study published this May on the appeal of “superfluous neuroscience information.” In it, Hodges and her colleagues presented students with a variety of explanations for various psychological phenomena. Some of these explanations were not really explanations at all, but rather just a restatement of the facts already presented. The students considered explanations for various quirks of human behavior from the fields of social science, biological science, and neuroscience, and rated how convincing they found each explanation. “The social sciences would refer to something about how people were raised, and the hard-science explanation referred to changes in DNA, the structure of DNA,” Hodges explained to Jarrett. The neuroscience explanation, on the other hand, would pretty much just name an area of the brain thought to be associated with the behavior at hand and leave matters at that, without really explaining anything. Even still, Hodges said, the “neuroscience explanations always came out on top — better than no explanation, better than social science, better than the hard science.” © 2015, New York Media LLC
Link ID: 21552 - Posted: 10.23.2015
By Karen Weintraub The short answer is: not yet, but treatments are getting better. Getting older is the leading risk factor for age-related macular degeneration, the leading cause of vision loss in the United States. Macular degeneration comes in two forms: dry and wet. The dry form is milder and usually has no symptoms, but it can degenerate into the wet form, which is characterized by the growth of abnormal blood vessels in the back of the eye, potentially causing blurriness or vision loss in the center of the field of vision. The best treatment for wet macular degeneration is prevention, said Dr. Rahul N. Khurana, a clinical spokesman for the American Academy of Ophthalmology and a retina specialist practicing in Mountain View, Calif. Not smoking, along with eating dark green vegetables and at least two servings of fish a week, may help reduce the risk of macular degeneration, he said. An annual eye exam can catch macular degeneration while it is still in the dry form, Dr. Khurana said, and vitamins can help prevent it from progressing into the wet form, the main cause of vision loss. Dr. Joan W. Miller, chief of ophthalmology at Massachusetts Eye and Ear, said anyone with a family history of the disease should get a retina check at age 50. People should also get an eye exam if they notice problems like trouble adjusting to the dark or needing more light to read. The federally funded Age-Related Eye Disease Study, published in 2001 and updated in 2013, found that people at high risk for advanced age-related macular degeneration could cut that risk by about 25 percent by taking a supplement that included 500 milligrams of vitamin C, 400 I.U.s of vitamin E, 10 milligrams of lutein, 2 milligrams of zeaxanthin, 80 milligrams of zinc, and 2 milligrams of copper. © 2015 The New York Times Company
Link ID: 21551 - Posted: 10.23.2015
By Hanae Armitage CHICAGO, ILLINOIS—Aside from a few animals—like pythons and vampire bats—that can sense infrared light, the world of this particular electromagnetic radiation has been off-limits to most creatures. But now, researchers have engineered rodents to see infrared light by implanting sensors in their visual cortex—a first-ever feat announced here yesterday at the annual meeting of the Society for Neuroscience. Before they wired rats to see infrared light, Duke University neuroscientist Miguel Nicolelis and his postdoc Eric Thomson engineered them to feel it. In 2013, they surgically implanted a single infrared-detecting electrode into an area of the rat’s brain that processes touch called the somatosensory cortex. The other end of the sensor, outside the rat’s head, surveyed the environment for infrared light. When it picked up infrared, the sensor sent electrical messages to the rats’ brains that seemed to give them a physical sensation. At first, the rats would groom and rub their whiskers repeatedly whenever the light went on. But after a short while, they stopped fidgeting. They even learned to associate infrared with a reward-based task in which they followed the light to a bowl of water. In the new experiment, the team inserted three additional electrodes, spaced out equally so that the rats could have 360 degrees of infrared perception. When they were primed to perform the same water-reward task, they learned it in just 4 days, compared to 40 days with the single implant. “Frankly, this was a surprise,” Thomson says. “I thought it would be really confusing for [the rats] to have so much stimulation all over their brain, rather than [at] one location.” © 2015 American Association for the Advancement of Science.
By Roni Jacobson After many lawsuits and a 2012 U.S. Department of Justice settlement, last month an independent review found that antidepressant drug Paxil (paroxetine) is not safe for teenagers. The finding contradicts the conclusions of the initial 2001 drug trial, which the manufacturer GlaxoSmithKline had funded, then used its results to market Paxil as safe for adolescents. The original trial, known as Study 329, is but one high-profile example of pharmaceutical industry influence known to pervade scientific research, including clinical trials the U.S. Food and Drug Administration requires pharma companies to fund in order to assess their products. For that reason, people who read scientific papers as part of their jobs have come to rely on meta-analyses, supposedly thorough reviews summarizing the evidence from multiple trials, rather than trust individual studies. But a new analysis casts doubt on that practice as well, finding that the vast majority of meta-analyses of antidepressants have some industry link, with a corresponding suppression of negative results. The latest study, published in the Journal of Clinical Epidemiology, which evaluated 185 meta-analyses, found that one third of them were written by pharma industry employees. “We knew that the industry would fund studies to promote its products, but it’s very different to fund meta-analyses,” which “have traditionally been a bulwark of evidence-based medicine,” says John Ioannidis, an epidemiologist at Stanford University School of Medicine and co-author of the study. “It’s really amazing that there is such a massive influx of influence in this field.” © 2015 Scientific American
Link ID: 21546 - Posted: 10.22.2015
In a study of mice, scientists discovered that a brain region called the thalamus may be critical for filtering out distractions. The study, published in Nature and partially funded by the National Institutes of Health, paves the way to understanding how defects in the thalamus might underlie symptoms seen in patients with autism, attention deficit hyperactivity disorder (ADHD), and schizophrenia. “We are constantly bombarded by information from our surroundings,” said James Gnadt, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “This study shows how the circuits of the brain might decide which sensations to pay attention to.” Thirty years ago Dr. Francis Crick proposed that the thalamus “shines a light” on regions of the cortex, which readies them for the task at hand, leaving the rest of the brain’s circuits to idle in darkness. “We typically use a very small percentage of incoming sensory stimuli to guide our behavior, but in many neurological disorders the brain is overloaded,” said Michael Halassa, M.D., Ph.D., the study’s senior author and an assistant professor at New York University’s Langone Medical Center. “It gets a lot of sensory input that is not well-controlled because this filtering function might be broken.” Neuroscientists have long believed that an area at the very front of the brain called the prefrontal cortex (PFC) selects what information to focus on, but how this happens remains unknown. One common theory is that neurons in the PFC do this by sending signals to cells in the sensory cortices located on the outer part of the brain. However, Dr. Halassa’s team discovered that PFC neurons may instead tune the sensitivity of a mouse brain to sights and sounds by sending signals to inhibitory thalamic reticular nucleus (TRN) cells located deep inside the brain.
Link ID: 21545 - Posted: 10.22.2015