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By SINDYA N. BHANOO Climate change may affect wood rats in the Mojave Desert in a most unusual way. A new study finds that warmer weather reduces their ability to tolerate toxins in the creosote bush, which they rely on for sustenance. The consequences may be dire for the wood rats. “There’s not much more they can eat out there,” said Patrice Kurnath, a biologist at the University of Utah and one of the study’s authors. She and her colleagues reported their findings in Proceedings of the Royal Society B: Biological Sciences. The leaves of the creosote bush contain a resin full of toxic compounds. They are known to cause kidney cysts and liver failure in laboratory rats. Wild wood rats, however, generally tolerate the poisons. Ms. Kurnath and her colleagues monitored the wood rats as they ate the leaves in warmer temperatures — around 83 degrees Fahrenheit. Although highs in the Mojave can reach the 80s and 90s during the summer, much of the year is cooler. The rats became less tolerant of the toxins and began to lose weight. The reason may have to do with how the liver functions in warmer weather, Ms. Kurnath said. The liver is the body’s primary detoxifying organ. When a mammalian liver is active, it increases internal body temperature. “In warmer weather, maybe you’re not producing huge amounts of heat and you’re not breaking down the toxins,” Ms. Kurnath said. © 2016 The New York Times Company
By Emily Underwood In 2008, in El Cajon, California, 30-year-old John Nicholas Gunther bludgeoned his mother to death with a metal pipe, and then stole $1378 in cash, her credit cards, a DVD/VCR player, and some prescription painkillers. At trial, Gunther admitted to the killing, but argued that his conviction should be reduced to second-degree murder because he had not acted with premeditation. A clinical psychologist and neuropsychologist testified that two previous head traumas—one the result of an assault, the other from a drug overdose—had damaged his brain’s frontal lobes, potentially reducing Gunther’s ability to plan the murder, and causing him to act impulsively. The jury didn’t buy Gunther’s defense, however; based on other evidence, such as the fact that Gunther had previously talked about killing his mother with friends, the court concluded that he was guilty of first-degree murder, and gave him a 25-years-to-life prison sentence. Gunther’s case represents a growing trend, a new analysis suggests. Between 2005 and 2012, more than 1585 U.S. published judicial opinions describe the use of neurobiological evidence by criminal defendants to shore up their defense, according to a study published last week in the Journal of Law and the Biosciences by legal scholar Nita Farahany of Duke University in Durham, North Carolina, and colleagues. In 2012 alone, for example, more than 250 opinions cited defendants’ arguments that their “brains made them do it”—more than double the number of similar claims made in 2007. © 2016 American Association for the Advancement of Science
Keyword: Drug Abuse
Link ID: 21816 - Posted: 01.23.2016
Richard A. Friedman WHO among us hasn’t wanted to let go of anxiety or forget about fear? Phobias, panic attacks and disorders like post-traumatic stress are extremely common: 29 percent of American adults will suffer from anxiety at some point in their lives. Sitting at the heart of much anxiety and fear is emotional memory — all the associations that you have between various stimuli and experiences and your emotional response to them. Whether it’s the fear of being embarrassed while talking to strangers (typical of social phobia) or the dread of being attacked while walking down a dark street after you’ve been assaulted (a symptom of PTSD), you have learned that a previously harmless situation predicts something dangerous. It has been an article of faith in neuroscience and psychiatry that, once formed, emotional memories are permanent. Afraid of heights or spiders? The best we could do was to get you to tolerate them, but we could never really rid you of your initial fear. Or so the thinking has gone. The current standard of treatment for such phobias revolves around exposure therapy. This involves repeatedly presenting the feared object or frightening memory in a safe setting, so that the patient acquires a new safe memory that resides in his brain alongside the bad memory. As long as the new memory has the upper hand, his fear is suppressed. But if he is re-traumatized or re-exposed with sufficient intensity to the original experience, his old fear will awaken with a vengeance. This is one of the limitations of exposure therapy, along with the fact that it generally works in only about half of the PTSD patients who try it. Many also find it upsetting or intolerable to relive memories of assaults and other traumatizing experiences. © 2016 The New York Times Company
Link ID: 21815 - Posted: 01.23.2016
By Diana Kwon Stories of cannabis’s abilities to alleviate seizures have been around for about 150 years but interest in medical marijuana has increased sharply in the last decade with the help of legalization campaigns. Credit: ©iStock Charlotte Figi, an eight-year-old girl from Colorado with Dravet syndrome, a rare and debilitating form of epilepsy, came into the public eye in 2013 when news broke that medical marijuana was able to do what other drugs could not: dramatically reduce her seizures. Now, new scientific research provides evidence that cannabis may be an effective treatment for a third of epilepsy patients who, like Charlotte, have a treatment-resistant form of the disease. Last month Orrin Devinsky, a neurologist at New York University Langone Medical Center, and his colleagues across multiple research centers published the results from the largest study to date of a cannabis-based drug for treatment-resistant epilepsy in The Lancet Neurology. The researchers treated 162 patients with an extract of 99 percent cannabidiol (CBD), a nonpsychoactive chemical in marijuana, and monitored them for 12 weeks. This treatment was given as an add-on to the patients’ existing medications and the trial was open-label (everyone knew what they were getting). The researchers reported the intervention reduced motor seizures at a rate similar to existing drugs (a median of 36.5 percent) and 2 percent of patients became completely seizure free. Additionally, 79 percent of patients reported adverse effects such as sleepiness, diarrhea and fatigue, although only 3 percent dropped out of the study due to adverse events. “I was a little surprised that the overall number of side effects was quite high but it seems like most of them were not enough that the patients had to come off the medication,” says Kevin Chapman, a neurology and pediatric professor at the University of Colorado School of Medicine who was not involved in the study. “I think that [this study] provides some good data to show that it's relatively safe—the adverse effects were mostly mild and [although] there were serious adverse effects, it's always hard to know in such a refractory population whether that would have occurred anyway.” © 2016 Scientific American,
By Brian Owens Guy Rouleau, the director of McGill University’s Montreal Neurological Institute (MNI) and Hospital in Canada, is frustrated with how slowly neuroscience research translates into treatments. “We’re doing a really shitty job,” he says. “It’s not because we’re not trying; it has to do with the complexity of the problem.” So he and his colleagues at the renowned institute decided to try a radical solution. Starting this year, any work done there will conform to the principles of the “open- science” movement—all results and data will be made freely available at the time of publication, for example, and the institute will not pursue patents on any of its discoveries. Although some large-scale initiatives like the government-funded Human Genome Project have made all data completely open, MNI will be the first scientific institute to follow that path, Rouleau says. “It’s an experiment; no one has ever done this before,” he says. The intent is that neuroscience research will become more efficient if duplication is reduced and data are shared more widely and earlier. Opening access to the tissue samples in MNI’s biobank and to its extensive databank of brain scans and other data will have a major impact, Rouleau hopes. “We think that it is a way to accelerate discovery and the application of neuroscience.” After a year of consultations among the institute’s staff, pretty much everyone—about 70 principal investigators and 600 other scientific faculty and staff—has agreed to take part, Rouleau says. Over the next 6 months, individual units will hash out the details of how each will ensure that its work lives up to guiding principles for openness that the institute has developed. They include freely providing all results, data, software, and algorithms; and requiring collaborators from other institutions to also follow the open principles. © 2016 American Association for the Advancement of Science.
Link ID: 21813 - Posted: 01.23.2016
Timothy Egan This weekend, I’m going to the Mojave Desert, deep into an arid wilderness of a half-million acres, for some stargazing, bouldering and January sunshine on my public lands. I won’t be out of contact. I checked. If Sarah Palin says something stupid on Donald Trump’s behalf — scratch that. When Sarah Palin says something stupid on Donald Trump’s behalf, I’ll get her speaking-in-tongues buffoonery in real time, along with the rest of the nation. The old me would have despised the new me for admitting such a thing. I’ve tried to go on digital diets, fasting from my screens. I was a friend’s guest at a spa in Arizona once and had so much trouble being “mindful” that they nearly kicked me out. Actually, I just wanted to make sure I didn’t miss the Seahawks game, mindful of Seattle’s woeful offensive line. In the information blur of last year, you may have overlooked news of our incredibly shrinking attention span. A survey of Canadian media consumption by Microsoft concluded that the average attention span had fallen to eight seconds, down from 12 in the year 2000. We now have a shorter attention span than goldfish, the study found. Attention span was defined as “the amount of concentrated time on a task without becoming distracted.” I tried to read the entire 54-page report, but well, you know. Still, a quote from Satya Nadella, the chief executive officer of Microsoft, jumped out at me. “The true scarce commodity” of the near future, he said, will be “human attention.” Putting aside Microsoft’s self-interest in promoting quick-flash digital ads with what may be junk science, there seems little doubt that our devices have rewired our brains. We think in McNugget time. The trash flows, unfiltered, along with the relevant stuff, in an eternal stream. And the last hit of dopamine only accelerates the need for another one. © 2016 The New York Times Company
Link ID: 21812 - Posted: 01.23.2016
Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.
Link ID: 21811 - Posted: 01.23.2016
By Elizabeth Pennisi PACIFIC GROVE, CALIFORNIA—Bats have an uncanny ability to track and eat insects on the fly with incredible accuracy. But some moths make these agile mammals miss their mark. Tiger moths, for example, emit ultrasonic clicks that jam bat radar. Now, scientists have shown that hawk moths (above) and other species have also evolved this behavior. The nocturnal insects—which are toxic to bats—issue an ultrasonic “warning” whenever a bat is near. After a few nibbles, the bat learns to avoid the noxious species altogether. The researchers shot high-speed videos of bat chases in eight countries over 4 years. Their studies found that moths with an intact sound-producing apparatus—typically located at the tip of the genitals—were spared, whereas those silenced by the researchers were readily caught. As the video shows, when the moths hear the bat’s clicks intensifying as it homes in, they emit their own signal, causing the bat to veer off at the last second. It could be that, like the tiger moths, the hawk moths are jamming the bat’s signal. But, because most moth signals are not the right type to interfere with the bat’s, the researchers say it’s more likely that the bat recognizes the signal and avoids the target on its own. Presenting here last week at a meeting of the American Society of Naturalists, the researchers say this signaling ability has evolved three times in hawk moths and about a dozen more times overall among other moths. © 2016 American Association for the Advancement of Science
Link ID: 21810 - Posted: 01.23.2016
By Melissa Dahl It’s the fifth inning and the Tampa Bay Rays are beating the Cleveland Indians 6–2 when Cleveland’s relief pitcher Nick Hagadone steps in. Alas, Hagadone does little to turn around the Indians’ luck that day, closing out the long inning with a score of 10–2. Hagadone, apparently frustrated by his own lackluster performance, heads to the clubhouse and, on the way there, punches a door with his left fist — the fist that is, unfortunately, connected to his pitching arm. That momentary impulse would cost him dearly. Hagadone required surgery and eight months’ recovery time — and, to add insult to a literal injury, his team also relegated him to the minor leagues, a move that shrank his annual salary by more than 80 percent. When asked about what could possibly explain an action like this in a usually easy-going guy, the Indians’ team psychologist, Charlie Maher, could only offer variations on this: “He just snapped.” Unless you are also a relief pitcher in the major leagues, you will likely never be in exactly this situation. But how many times have you reacted aggressively, even violently, in a way that felt almost out of your control? You hurl your smartphone across the room, or you unleash a stream of expletives in a manner that would seem to a calmer, rational mind to be disproportionate to the situation at hand. “I just snapped” is how we explain it to ourselves and others, and then we move on. The phrase has become such a cliché that it’s easy to forget that it doesn’t really explain much of anything. What’s behind this impulsive, immediately regrettable behavior? R. Douglas Fields, a senior investigator at the National Institutes of Health, sought out an explanation in his new book, Why We Snap: Understanding the Rage Circuit in Your Brain, which includes the Hagadone story recounted above. © 2016, New York Media LLC
By Kerry Klein With their suction cup mouths filled with concentric circles of pointy teeth that suck the body fluid of unsuspecting victims, lampreys may seem like the stuff of horror movies. And indeed the 50-centimeter-long, eellike creatures can wreak havoc on freshwater communities when they invade from the sea, with a single sea lamprey able to kill 18 kilograms of fish in its lifetime. Now, the U.S. government has approved of a new way to combat these fearsome fish by using their own sense of smell against them. Sea lampreys are a particular problem in the Great Lakes regions of the United States and Canada. They hitchhiked into the region more than a century ago, likely attaching themselves to ships or fish that traveled along shipping channels from the Atlantic Ocean. Although most lampreys are mere parasites in their native habitats, those in the Great Lakes are far worse, says Nicholas Johnson, a research ecologist at the U.S. Geological Survey’s Hammond Bay Biological Station on Lake Huron in Millersburg, Michigan. “They kill their host, they get too big, they eat too much,” he says. “They’re really more of a predator.” After the toothy invaders proliferated in the mid-20th century, ecosystems all but collapsed, taking prosperous fishing and tourism industries with them. “It’s fair to say that lamprey[s] changed the way of life in the region,” says Marc Gaden of the Great Lakes Fishery Commission, a joint U.S. and Canadian organization based in Ann Arbor, Michigan, that’s tasked with managing the rebounding ecosystems. “Just about every fishery management decision that we make to this day has to take lamprey into consideration.” © 2016 American Association for the Advancement of Science
By Geoffrey Giller The experience of seeing a lightning bolt before hearing its associated thunder some seconds later provides a fairly obvious example of the differential speeds of light and sound. But most intervals between linked visual and auditory stimuli are so brief as to be imperceptible. A new study has found that we can glean distance information from these minimally discrepant arrival times nonetheless. In a pair of experiments at the University of Rochester, 12 subjects were shown projected clusters of dots. When a sound was played about 40 or 60 milliseconds after the dots appeared (too short to be detected consciously), participants judged the clusters to be farther away than clusters with simultaneous or preceding sounds. Philip Jaekl, the lead author of the study and a postdoctoral fellow in cognitive neuroscience, says it makes sense that the brain would use all available sensory information for calculating distance. “Distance is something that's very difficult to compute,” he explains. The study was recently published in the journal PLOS ONE. Aaron Seitz, a professor of psychology and neuroscience at the University of California, Riverside, who was not involved in the work, says the results may be useful clinically, such as by helping people with amblyopia (lazy eye) improve their performance when training to see with both eyes. And there might be other practical applications, including making virtual-reality environments more realistic. “Adding in a delay,” says Nick Whiting, a VR engineer for Epic Games, “can be another technique in our repertoire in creating believable experiences.” © 2016 Scientific American,
Link ID: 21807 - Posted: 01.21.2016
by Emily Reynolds We know more about what the brain does when it's active than we do when it's at rest. It makes sense -- much neuroscientific research has looked to understand particular (and active) processes. James Kozloski, a researcher at IBM, has investigated what the brain does when it's resting -- what he calls 'the Grand Loop'. "The brain consumes a great amount of energy doing nothing. It's a great mystery of neuroscience," Kozloski told PopSci. He argued that around 90 percent of the energy used by the brain remained "unaccounted for". He believes that the brain is constantly 'looping signals', retracing neural pathways over and over again. It's a "closed loop", according to Kozloski, meaning it isn't reliant on external inputs as much of the brain's activity is. Kozloski tested his theory by running his model through IBM's neural tissue simulator and found that it could potentially account for genetic mutations such as Huntington's. He argued that information created by one mutated gene could, through the 'Grand Loop', affect an entire neural pathway. So what happens when our brain is at work? And how does expending energy affect our neural processes? Much historic research into anxiety has found that people tend to exert more energy or force when they're being watched -- something that leads to slip-ups or mistakes under pressure.
By David Shultz It’s a familiar image: a group monkeys assembled in a line, picking carefully through each other’s hair, eating any treasures they might find. The grooming ritual so common in many primate species serves to both keep the monkeys healthy as well as reinforce social structures and bonds. But according to new research on vervet monkeys (Chlorocebus pygerythrus, seen above), the behavior may also improve a pelt’s insulation by fluffing it up like a duvet, scientists report in the American Journal of Primatology. To test the difference between groomed or ungroomed fur, the team manually combed vervet monkey pelts either with or against the grain for 50 strokes. The fluffed up “backcombed” pelts simulated a recently groomed monkey, whereas the flattened pelts simulated an ungroomed state. Using a spectrophotometer, the researchers then measured how much light was reflected by each pelt and calculated the pelt’s total insulation. They found that a thicker, fluffier coat could improve a monkey’s insulation by up to 50%, keeping the animal warmer in the cold and cooler in the heat. Thus, grooming may help the vervets maintain a constant body temperature with less effort, freeing up more energy for sex, foraging, and participating in monkey society. In the face of climate change, the authors note, such flexibility could soon become enormously important. © 2016 American Association for the Advancement of Science.
A map for other people’s faces has been discovered in the brain. It could help explain why some of us are better at recognising faces than others. Every part of your body that you can move or feel is represented in the outer layer of your brain. These “maps”, found in the motor and sensory cortices (see diagram, below), tend to preserve the basic spatial layout of the body – neurons that represent our fingers are closer to neurons that represent our arms than our feet, for example. The same goes for other people’s faces, says Linda Henriksson at Aalto University in Helsinki, Finland. Her team scanned 12 people’s brains while they looked at hundreds of images of noses, eyes, mouths and other facial features and recorded which bits of the brain became active. This revealed a region in the occipital face area in which features that are next to each other on a real face are organised together in the brain’s representation of that face. The team have called this map the “faciotopy”. The occipital face area is a region of the brain known to be involved in general facial processing. “Facial recognition is so fundamental to human behaviour that it makes sense that there would be a specialised area of the brain that maps features of the face,” she says. © Copyright Reed Business Information Ltd.
By David Shultz A rat navigating a maze has to rank somewhere near the top of science tropes. Now, scientists report that they’ve developed an analogous test for humans—one that involves driving through a virtual landscape in a simulated car. The advance, they say, may provide a more sensitive measure for detecting early signs of Alzheimer’s disease. “I think it’s a very well-done study,” says Keith Vossel, a translational neuroscientist at the University of California, San Francisco (UCSF), who was not involved with the work. In the rodent version of the so-called Morris Maze Test, researchers fill a large cylindrical container with water and place a platform just above the waterline. A scientist then places a rat into the tank, and the rodent must swim to the platform to avoid drowning. The experimenter then raises the water level just above the height of the platform and adds a compound to the water to make it opaque. The trial is repeated, but now the rat must find the platform without seeing it, using only its memory of where the safe zone exists relative to the tank’s walls and the surrounding environment. In subsequent trials, researchers place the rat at different starting points along the tank’s edge, but the platform stays put. In essence, the task requires the rat to move to a specific but invisible location within a circular arena from different starting points. © 2016 American Association for the Advancement of Science.
Link ID: 21803 - Posted: 01.20.2016
The Chamorro people of the Pacific island of Guam know it as lytigo-bodig. For decades, they have been struck down by a mysterious illness that resembles the muscle-wasting disease amyotrophic lateral sclerosis (ALS), Parkinson’s disease and Alzheimer’s-like dementia. It now looks like we have a clue that could point to a way of slowing its development. Lytigo-bodig is a progressive disease. ALS symptoms arrive when people are in their mid-40s and early 50s. By the time they reach their 60s, they also have the shaking and lack of coordination that characterises Parkinson’s, before the cognitive problems associated with dementia also set in. “Initially they stumble a bit, but as their muscles wither, they need help with eating and going to the toilet, as well as having difficulty swallowing and breathing,” says Paul Cox of the Institute for Ethnomedicine in Wyoming. For a long time, a chemical called BMAA, found in the cycad seeds that the Chamorro grind up to make flour, has been suspected as the cause of the disease. The toxin builds up in the cyanobacteria that grow in the roots of cycad plants. It also accumulates in the tissue of seed-eating flying foxes, which the Chamorro hunt and eat. To see if they could confirm BMAA as the culprit, Cox fed fruit spiked with the toxin to vervet monkeys for 140 days. They estimated this was equivalent to the dose a typical islander might get over a lifetime. Although they didn’t show cognitive problems, the animals did develop brain abnormalities called tau tangles and deposits of amyloid plaque. The density and placement of these abnormalities were similar to those seen in the islanders. “The structure of the pathology is almost identical,” says Cox. “We were stunned.” © Copyright Reed Business Information Ltd.
It seems like the ultimate insult, but getting people with brain injuries to do maths may lead to better diagnoses. A trial of the approach has found two people in an apparent vegetative state that may be conscious but “locked-in”. People who are in a vegetative state are awake but have lost all cognitive function. Occasionally, people diagnosed as being in this state are actually minimally conscious with fleeting periods of awareness, or even locked-in. This occurs when they are totally aware but unable to move any part of their body. It can be very difficult to distinguish between each state, which is why a team of researchers in China have devised a brain-computer interface that tests whether people with brain injuries can perform mental arithmetic – a clear sign of conscious awareness. The team, led by Yuanqing Li at South China University of Technology and Jiahui Pan at the South China Normal University in Guangzhou showed 11 people with various diagnoses a maths problem on a screen. This was followed by two possible answers flickering at frequencies designed to evoke different patterns of brain activity. Frames around each number also flashed several times. The participants were asked to focus on the correct answer and count the number of times its frame flashed. The brain patterns from the flickering answers together with the detection of another kind of brain signal that occurs when someone counts, enabled a computer to tell which answer, if any, the person was focusing on. © Copyright Reed Business Information Ltd.
Link ID: 21801 - Posted: 01.19.2016
By Emily Underwood Roughly half of Americans use marijuana at some point in their lives, and many start as teenagers. Although some studies suggest the drug could harm the maturing adolescent brain, the true risk is controversial. Now, in the first study of its kind, scientists have analyzed long-term marijuana use in teens, comparing IQ changes in twin siblings who either used or abstained from marijuana for 10 years. After taking environmental factors into account, the scientists found no measurable link between marijuana use and lower IQ. “This is a very well-conducted study … and a welcome addition to the literature,” says Valerie Curran, a psychopharmacologist at the University College London. She and her colleagues reached “broadly the same conclusions” in a separate, nontwin study of more than2000 British teenagers, published earlier this month in the Journal of Psychopharmacology, she says. But, warning that the study has important limitations, George Patton, a psychiatric epidemiologist at the University of Melbourne in Australia, adds that it in no way proves that marijuana—particularly heavy, or chronic use —is safe for teenagers. Most studies that linked marijuana to cognitive deficits, such as memory loss and low IQ, looked at a single “snapshot” in time, says statistician Nicholas Jackson of the University of Southern California in Los Angeles, lead author of the new work. That makes it impossible to tell which came first: drug use or poor cognitive performance. “It's a classic chicken-egg scenario,” he says. © 2016 American Association for the Advancement of Science.
Finding out what’s going on in an injured brain can involve several rounds of surgery, exposed wounds and a mess of wires. Perhaps not for much longer. A device the size of a grain of rice can monitor the brain’s temperature and pressure before dissolving without a trace. “This fully degradable sensor is definitely an impressive feat of engineering,” says Frederik Claeyssens, a biomaterials scientist at the University of Sheffield, UK. The device is the latest creation from John Rogers’s lab at the University of Illinois at Urbana-Champaign. They came up with the idea of a miniature dissolvable brain monitor after speaking to neurosurgeons about the difficulties of monitoring brain temperature and pressure in people with traumatic injuries. Unwieldy wires These vital signs are currently measured via an implanted sensor connected to an external monitor. “It works, but the wires coming out of the head limit physical movement and provide a nidus for infection. You can cause additional damage when you pull them out,” says Rogers. It would be better to use a wireless device that doesn’t need to be extracted, he says. So Rogers’s team developed an electronic monitor about a tenth of a millimetre wide and a millimetre long made of silicon and a polymer. These materials, used in tiny amounts, are eventually broken down by the body, and don’t trigger any harmful effects, says Rogers. “The materials individually are safe. The total amount is very small. It’s about 1000 times less than what you’d have in a vitamin tablet.” © Copyright Reed Business Information Ltd.
Keyword: Brain imaging
Link ID: 21799 - Posted: 01.19.2016
By SINDYA N. BHANOO Male zebra finches learn their courtship songs from their fathers. Now, a new study details the precise changes in brain circuitry that occur during that process. As a young male listens to his father’s song, networks of brain cells are activated that the younger bird will use later to sing the song himself, researchers have found. As the learning process occurs, inhibitory cells suppress further activity in the area and help sculpt the song into a permanent memory. “These inhibitory cells are really smart — once you’ve gotten a part of the song down, the area gets locked,” said Michael Long, a neuroscientist at NYU Langone Medical Center and an author of the new study, which appears in the journal Science. Zebra finches learn their courtship song from their fathers and reach sexual maturity in about 100 days. At this point, they ignore their fathers’ tutoring altogether, Dr. Long said. In their study, he and his colleagues played recorded courtship songs to young and old birds and monitored neural activity in their brains. In sexually mature birds, the courtship song did not elicit any neural response. Understanding the role of the inhibitory cells in the brain could help researchers develop ways to manipulate this network, Dr. Long said. “Maybe we could teach old birds new tricks,” he said. “And extrapolating widely, maybe we could even do this in mammals, maybe even humans, and enrich learning.” © 2016 The New York Times Company