Two pioneers in the study of neural signaling and three researchers responsible for modern cochlear implants are winners of The Albert and Mary Lasker Foundation’s annual prize, announced today. The prestigious award honoring contributions in the medical sciences is often seen as a hint at future Nobel contenders. The prizes for basic and clinical research each carry a $250,000 honorarium. Richard Scheller of the biotech company Genentech and Thomas Südhof of Stanford University in Palo Alto, California, got their basic research Laskers for discovering the mechanisms behind rapid the release of neurotransmitters—the brain’s chemical messengers—into the space between neurons. This process underlies all communication among brain cells, and yet it was “a black box” before Scheller and Südhof’s work, says their colleague Robert Malenka, a synaptic physiologist at Stanford. The two worked independently in the late 1980s to identify individual proteins that mediate the process, and their development of genetically altered mice lacking these proteins was “an ambitious and high-risk approach,” Malenka says. Although “they weren’t setting out to understand any sort of disease,” their discoveries have helped unravel the genetic basis for neurological disorders such as Parkinson’s disease. This year’s clinical research prizes went to Graeme Clark, Ingeborg Hochmair, and Blake Wilson for their work to restore hearing to the deaf. In the 1970s, Hochmair and Clark of the cochlear implant company MED-EL in Innsbruck, Austria, and the University of Melbourne, respectively, were the first to insert multiple electrodes into the human cochlea to stimulate nerves that respond to different frequencies of sound. © 2012 American Association for the Advancement of Science

Keyword: Hearing; Robotics
Link ID: 18625 - Posted: 09.10.2013

By RONI JACOBSON We have seven deadly sins, seven days of the week, seven seas, seven dwarfs. The recurrence of the number seven so impressed the cognitive psychologist George A. Miller that, in an oft-cited paper in 1956, he wrote, “My problem is that I have been persecuted by an integer.” Miller went on to describe several experiments where seven pieces of information — plus or minus two — appeared to be the limit of what our minds could retain in the short term. Since then, Miller’s theory — that our short-term memory can hold about seven items before we start to forget them — has been refined. It is now understood that the capacity of short-term memory depends on several factors, including age, attention and the type of information presented. For instance, long words like “onomatopoeia” and “reciprocate” take up more memory span than short words like “cat” and “ball.” Grouping smaller bits of information into a meaningful unit, like a word of many syllables or an abstract concept, is called “chunking,” and our ability to retain information decreases as the chunk becomes more complex. Psychologists now believe that we can recall about four chunks of information at a time, which works out to approximately six letters, five one-syllable words and seven digits. As for the ubiquity of the number seven, Miller came to suspect that that is just a coincidence. © 2013 The New York Times Company

Keyword: Learning & Memory
Link ID: 18624 - Posted: 09.10.2013

By Athena Andreadis Recently, two studies surfaced almost simultaneously that led to exclamations of “Vulcan mind meld!”, “Zombie armies!” and “Brains in jars!” One is the announcement by Rajesh Rao and Andrea Stocco of Washington U. that they “achieved the first human-to-human brain interface”. The other is the Nature paper by Madeline Lancaster et al about stem-cell-derived “organoids” that mimic early developmental aspects of the human cortex. My condensed evaluation: the latter is far more interesting and promising than the former, which doesn’t quite do what people (want to) think it’s doing. The purported result of brain interfacing hit many hot buttons that have been staples of science fiction and Stephen King novels: primarily telepathy, with its fictional potential for non-consensual control. Essentially, the sender’s EEG (electroencephalogram) output was linked to the receiver’s TMS (transcranial magnetic stimulation) input. What the experiment actually did is not send a thought but induce a muscle twitch; nothing novel, given the known properties of the two technologies. The conditions were severely constrained to produce the desired result and I suspect the outcome was independent of the stimulus details: the EEG simply recorded that a signal had been produced and the TMS apparatus was positioned so that a signal would elicit a movement of the right hand. Since both sender and receiver were poised over a keyboard operating a video game, the twitch was sufficient to press the space bar, programmed by the game to fire a cannon. © 2013 Scientific American

Keyword: Robotics
Link ID: 18623 - Posted: 09.10.2013

By Nathan Seppa A tiny probe equipped with a laser might reveal what the human eye doesn’t always see: the difference between a tumor and healthy tissue. A new study suggests the device might provide brain surgeons with a roadmap as they go about the delicate business of removing tumors. Surgeons try to excise as much of brain tumors as possible, but they risk harming the patient if they remove healthy tissue. “This problem,” says surgeon Daniel Orringer of the University of Michigan in Ann Arbor, “has vexed brain surgeons for as long as they have taken out tumors,” since the first half of the 20th century. “Basically, we do it by feel — the texture, color and vascularity of the tissues. Tumors tend to bleed a little more than normal brain.” Although removing and testing tissue samples, or biopsies, can help to characterize the tissue at the tumor margins, it’s a cumbersome and time-consuming process. In the new study, Orringer and his colleagues instead exposed such borderline brain tissues to a weak laser. Then they used Raman spectroscopy, a technique that reveals vibrations of specific chemical bonds in tissues. The revved up form of Raman spectroscopy that the researchers used is sensitive enough to distinguish between proteins and lipids. Since tumors are higher in protein than healthy brain tissue, the authors designed the technique to present protein signatures as blue images on a screen, and lipids as green. © Society for Science & the Public 2000 - 2013

Keyword: Brain imaging
Link ID: 18622 - Posted: 09.09.2013

By ERIC R. KANDEL THESE days it is easy to get irritated with the exaggerated interpretations of brain imaging — for example, that a single fMRI scan can reveal our innermost feelings — and with inflated claims about our understanding of the biological basis of our higher mental processes. Such irritation has led a number of thoughtful people to declare that we can never achieve a truly sophisticated understanding of the biological foundation of complex mental activity. In fact, recent newspaper articles have argued that psychiatry is a “semi-science” whose practitioners cannot base their treatment of mental disorders on the same empirical evidence as physicians who treat disorders of the body can. The problem for many people is that we cannot point to the underlying biological bases of most psychiatric disorders. In fact, we are nowhere near understanding them as well as we understand disorders of the liver or the heart. But this is starting to change. Consider the biology of depression. We are beginning to discern the outlines of a complex neural circuit that becomes disordered in depressive illnesses. Helen Mayberg, at Emory University, and other scientists used brain-scanning techniques to identify several components of this circuit, two of which are particularly important. One is Area 25 (the subcallosal cingulate region), which mediates our unconscious and motor responses to emotional stress; the other is the right anterior insula, a region where self-awareness and interpersonal experience come together. These two regions connect to the hypothalamus, which plays a role in basic functions like sleep, appetite and libido, and to three other important regions of the brain: the amygdala, which evaluates emotional salience; the hippocampus, which is concerned with memory; and the prefrontal cortex, which is the seat of executive function and self-esteem. All of these regions can be disturbed in depressive illnesses. © 2013 The New York Times Company

Keyword: Brain imaging; Depression
Link ID: 18621 - Posted: 09.09.2013

by Jon White Ever tried beetroot custard? Probably not, but your brain can imagine how it might taste by reactivating old memories in a new pattern. Helen Barron and her colleagues at University College London and Oxford University wondered if our brains combine existing memories to help us decide whether to try something new. So the team used an fMRI scanner to look at the brains of 19 volunteers who were asked to remember specific foods they had tried. Each volunteer was then given a menu of 13 unusual food combinations – including beetroot custard, tea jelly, and coffee yoghurt – and asked to imagine how good or bad they would taste, and whether or not they would eat them. "Tea jelly was popular," says Barron. "Beetroot custard not so much." When each volunteer imagined a new combination, they showed brain activity associated with each of the known ingredients at the same time. It is the first evidence to suggest that we use memory combination to make decisions, says Barron. Journal reference: Nature Neuroscience, doi: 10.1038/nn.3515 © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory; Brain imaging
Link ID: 18620 - Posted: 09.09.2013

By Josh Shaffer DURHAM It’s not often that the high-minded world of neuroscience collides with the corny, old-fashioned art of ventriloquism. One depends on dummies; the other excludes them. But a Duke University study uses puppet-based comedy to demonstrate the complicated inner workings of the brain and shows what every ventriloquist knows: The eye is more convincing than the ear. The study, which appears in the journal PLOS ONE, seeks to explain how the brain combines information coming from two different senses. How, asks Duke psychology and neuroscience professor Jennifer Groh, does the brain determine where a sound is coming from? In your eyes, the retina takes a snapshot, she said. It makes a topographic image of what’s in front of you. But the ears have nothing concrete to go on. They have to rely on how loud the sound is, how far away and from what direction. That’s where a ventriloquist comes in, providing a model for this problem. With a puppet, the noise and the movement are coming from different places. So how does the brain fix this and choose where to look? Duke researchers tested their hypotheses on 11 people and two monkeys, placing them in a soundproof booth.

Keyword: Attention; Vision
Link ID: 18619 - Posted: 09.09.2013

by Andy Coghlan Smokers keen to quit are just as likely to be successful if they use electronic cigarettes as they are with nicotine patches, the "gold standard" quitting aid. The findings come ahead of a critical debate in the European Parliament on 8 October to decide whether e-cigarettes should be regulated as medicinal products, which would drastically reduce their availability. When smokers attempt to quit, it is the cutting out of nicotine – the addictive component of tobacco – that triggers withdrawal symptoms. E-cigarettes, which physically resemble real cigarettes, provide a compensatory nicotine hit, without the toxic brew of carcinogenic compounds. Previous studies conducted on e-cigarettes alone have shown that they help smokers quit, but no one knew if they performed as well as nicotine patches. To find out, the New Zealand government funded a head-to-head comparison study. Chris Bullen and his colleagues at the National Institute for Health Innovation in Auckland gave e-cigarettes to 289 smokers who were trying to quit. A separate group of 295 people were given nicotine patches, while 73 received dummy nicotine-free e-cigarettes. Six months later, the team asked participants if their attempts to quit had been a success. Those who had used the nicotine e-cigarettes had the highest success rate: 7.3 per cent had managed to stay away from tobacco. Of the nicotine patch users, 5.8 per cent had quit. And of those taking the placebo around 4 per cent were successful. © Copyright Reed Business Information Ltd.

Keyword: Drug Abuse
Link ID: 18618 - Posted: 09.09.2013

Brian Owens Gut bacteria from lean mice can invade the guts of obesity-prone cage-mates and help their new hosts to fight weight gain. Researchers led by Jeffrey Gordon, a biologist at Washington University in St. Louis, Missouri, set out to find direct evidence that gut bacteria have a role in obesity. The team took gut bacteria from four sets of human twins in which one of each pair was lean and one was obese, and introduced the microbes into mice bred to be germ-free. Mice given bacteria from a lean twin stayed slim, whereas those given bacteria from an obese twin quickly gained weight, even though all the mice ate about the same amount of food. The team wondered whether the gut microbiota of either group of mice would be influenced by mice with one type living in close quarters with animals harbouring the other type. So the scientists took mice with the ‘lean’ microbiota and placed them in a cage with mice with the ‘obese’ type before those mice had a chance to start putting on weight. “We knew the mice would readily exchange their microbes,” Gordon says — that is, eat each other’s faeces. Sure enough, the populations of bacteria in the obese-type mice changed to match those of their lean cage-mates, and their bodies remained lean, the team writes today in Science1. © 2013 Nature Publishing Group,

Keyword: Obesity
Link ID: 18617 - Posted: 09.07.2013

By Meghan Rosen Skinniness could be contagious. Gut bacteria from thin people can invade the intestines of mice carrying microbes from obese people. And these invaders can keep mice from getting tubby, researchers report in the Sept. 6 Science. “It’s very surprising,” says molecular microbiologist Andreas Schwiertz of the University of Giessen in Germany, who was not involved in the work. “It’s like a beneficial infection.” But the benefits come with a catch. The invading microbes drop in and get to work only when mice eat healthy food. Even fat-blocking bacteria can’t fight a bad diet, suggests study leader Jeffrey Gordon, a microbiologist at Washington University in St. Louis. In recent years, researchers have collected clues that suggest that gut microbes can tweak people’s metabolism. Fat and thin people have different microbes teeming in their intestines, for example. And normal-weight mice given microbes from obese mice pack on extra fat, says coauthor Vanessa Ridaura, also of Washington University. These and other hints have led researchers to experiment with fecal transplants to flush out bad gut microbes and dump in good ones. The transplants can clear up diarrhea and may even help some obese people regain insulin sensitivity. But feces can house dangerous microbes as well as friendly ones. “We want to make therapies that are more standardized — and more appealing,” says gastroenterologist Josbert Keller of the Haga Teaching Hospital in The Hague, Netherlands. © Society for Science & the Public 2000 - 2013

Keyword: Obesity
Link ID: 18616 - Posted: 09.07.2013

By Tamar Haspel, American eaters love a good villain. Diets that focus on one clear bad guy have gotten traction even as the bad guy has changed: fat, carbohydrates, animal products, cooked food, gluten. And now Robert Lustig, a pediatric endocrinologist at the University of California at San Francisco, is adding sugar to the list. His book “ Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease ” makes the case that sugar is almost single-handedly responsible for Americans’ excess weight and the illnesses that go with it. “Sugar is the biggest perpetrator of our current health crisis,” says Lustig, blaming it for not just obesity and diabetes but also for insulin resistance, cardiovascular disease, stroke, even cancer. “Sugar is a toxin,” he says. “Pure and simple.” His target is one particular sugar: fructose, familiar for its role in making fruit sweet. Fruit, though, is not the problem; the natural sugar in whole foods, which generally comes in small quantities, is blameless. The fructose in question is in sweeteners — table sugar, high-fructose corn syrup, maple syrup, honey and others — which are all composed of the simple sugars fructose and glucose, in about equal proportions. Although glucose can be metabolized by every cell in the body, fructose is metabolized almost entirely by the liver. There it can result in the generation of free radicals ( damaged cells that can damage other cells) and uric acid ( which can lead to kidney disease or gout ), and it can kick off a process called de novo lipogenesis, which generates fats that can find their way into the bloodstream or be deposited on the liver itself. These byproducts are linked to obesity, insulin resistance and the group of risk factors linked to diabetes, heart disease and stroke. (Lustig gives a detailed explanation of fructose metabolism in a well-viewed YouTube video called “Sugar: The Bitter Truth.”) © 1996-2013 The Washington Post

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 18615 - Posted: 09.07.2013

By Caitlin Kirkwood Do NOT EAT the chemicals. It is the #1 laboratory safety rule young scientists learn to never break and for good reason; it keeps lab citizens alive and unscathed. However, if it hadn’t been for the careless, rule-breaking habits of a few rowdy scientists ingesting their experiments, many artificial sweeteners may never have been discovered. Perhaps the strangest anecdote for artificial sweetener discovery, among tales of inadvertent finger-licking and smoking, is that of graduate student Shashikant Phadnis who misheard instructions from his advisor to ‘test’ a compound and instead tasted it. Rather than keeling over, he identified the sweet taste of sucralose, the artificial sweetener commonly known today as Splenda. Artificial sweeteners like Splenda, Sweet’N Low, and Equal provide a sweet taste without the calories. Around World War II, in response to a sugar shortage and evolving cultural views of beauty, the target consumer group for noncaloric sweetener manufacturers shifted from primarily diabetics to anyone in the general public wishing to reduce sugar intake and lose weight. Foods containing artificial sweeteners changed their labels. Instead of cautioning ‘only for consumption by those who must restrict sugar intake’, they read for those who ‘desire to restrict’ sugar. Today, the country is in the middle of a massive debate about the health implications of artificial sweeteners and whether they could be linked to obesity, cancer, and Alzheimer disease. It’s a good conversation to have because noncaloric sweeteners are consumed regularly in chewing gums, frozen dinners, yogurts, vitamins, baby food, and particularly in diet sodas. © 2013 Scientific American

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 18614 - Posted: 09.07.2013

Inner-ear problems could be a cause of hyperactive behaviour, research suggests. A study on mice, published in Science, said such problems caused changes in the brain that led to hyperactivity. It could lead to the development of new targets for behaviour disorder treatments, the US team says. A UK expert said the study's findings were "intriguing" and should be investigated further. Behavioural problems such as ADHD are usually thought to originate in the brain. But scientists have observed that children and teenagers with inner-ear disorders - especially those that affect hearing and balance - often have behavioural problems. However, no causal link has been found. The researchers in this study suggest inner-ear disorders lead to problems in the brain which then also affect behaviour. The team from the Albert Einstein College of Medicine of Yeshiva University in New York noticed some mice in the lab were particularly active - constantly chasing their tails. They were found to be profoundly deaf and have disorders of the inner ear - of both the cochlea, which is responsible for hearing, and the vestibular system, which is responsible for balance. The researchers found a mutation in the Slc12a2 gene, also found in humans. Blocking the gene's activity in the inner ears of healthy mice caused them to become increasingly active. BBC © 2013

Keyword: ADHD; Hearing
Link ID: 18613 - Posted: 09.07.2013

By Bruce Bower Strange things happen when bad singers perform in public. Comedienne Roseanne Barr was widely vilified in 1990 after she screeched the national anthem at a major league baseball game. College student William Hung earned worldwide fame and a recording contract in 2004 with a tuneless version of Ricky Martin’s hit song “She Bangs” on American Idol. Several singers at karaoke bars in the Philippines have been shot to death by offended spectators for mangling the melody of Frank Sinatra’s “My Way.” For all the passion evoked by pitch-impaired vocalists, surprisingly little is known about why some people are cringe-worthy crooners. But now a rapidly growing field of research is beginning to untangle the mechanics of off-key singing. The new results may improve scientists’ understanding of how musical abilities develop and help create a toolbox of teaching strategies for aspiring vocalists. Glimpses are also emerging into what counts as “in tune” to the mind’s ear. It seems that listeners are more likely to label stray notes as in tune when those notes are sung as opposed to played on a violin. Running through this new wave of investigations is a basic theme: There is one way to carry a tune and many ways to fumble it. “It’s kind of amazing that any of us can vocally control pitch enough to sing well,” says psychologist Peter Pfordresher of the University at Buffalo, New York. Still, only about 10 percent of adults sing poorly, several reports suggest (although some researchers regard that figure as an underestimate). Some of those tune-challenged crooners have tone deafness, a condition called amusia, which afflicts about 4 percent of the population. Genetic and brain traits render these folks unable to tell different musical notes apart or to recognize a tune as common as “Happy Birthday.” Amusia often — but curiously, not always — results in inept singing. Preliminary evidence suggests that tone-deaf individuals register pitch changes unconsciously, although they can’t consciously decide whether one pitch differs from another. © Society for Science & the Public 2000 - 2013

Keyword: Hearing
Link ID: 18612 - Posted: 09.07.2013

Kelly Servick If keeping the brain spry were as simple as pumping iron, everyone would want to own the ultimate piece of cognitive exercise equipment. But designing activities to reverse the mental effects of aging is tricky. A new video game created by neuroscientists shows promise in reversing some signs of decline. Now, the researchers behind it aim to prove that video game training can be more than the latest workout craze. Games designed to keep the brain healthy as it ages have found an eager audience. “Many, many people have gotten into the business,” says neuropsychologist Glenn Smith of the Mayo Clinic in Rochester, Minnesota. The brain does appear to be capable of changing its structure and developing new skills over the course of a lifetime. But not all the products on the market are designed using scientific knowledge of the aging brain, and their ability to make meaningful, lasting changes hasn’t been proven, says Smith, who studies games as treatment for early signs of dementia. “There’s an awful lot of skepticism out there,” he says. The heart of the issue is whether practicing a video game can strengthen skills that are useful away from a computer. Early research showed that people could improve on computerized memory and speed tasks in the lab, Smith says. But it’s not clear whether these gains translate to everyday life. A recent trend puts more value in games that target the underlying problem—the decline in ability to remember and react as people age. © 2012 American Association for the Advancement of Science.

Keyword: Alzheimers; Learning & Memory
Link ID: 18611 - Posted: 09.05.2013

R. Douglas Fields The Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative announced by US President Barack Obama in April seeks to map and monitor the function of neural connections in the entire brains of experimental animals, and eventually in the human cerebral cortex. Several researchers have raised doubts about the project, cautioning that mapping the brain is a much more complex endeavour than mapping the human genome, and its usefulness more uncertain. I believe that exploring neural networks and developing techniques with which to do so are important goals that should be vigorously supported. But simply scaling up current efforts to chart neural connections is unlikely to deliver the promised benefits — which include understanding perception, consciousness, how the brain produces memories, and the development of treatments for diseases such as epilepsy, depression and schizophrenia1. A major stumbling block is the project's failure to consider that although the human brain contains roughly 100 billion neurons, it contains billions more non-electrical brain cells called glia2. These reside outside the neuronal 'connectome' and operate beyond the reach of tools designed to probe electrical signalling in neurons. Dismissed as connective tissue when they were first described in the mid-1800s, glia have long been neglected in the quest to understand neuronal signalling. Research is revealing that glia can sense neuronal activity and control it3. Various studies also indicate that glia operate in diverse mental processes, for instance, in the formation of memories. They have a central role in brain injury and disease, and they are even at the root of various disorders — such as schizophrenia and Alzheimer's — previously presumed to be exclusively neuronal. That the word 'glia' was not uttered in any of the announcements of the BRAIN Initiative, nor written anywhere in the 'white papers' published in 2012 and 2013 in prominent journals outlining the ambitious plan1, 4, speaks volumes about the need for the community of neuroscientists behind the initiative to expand its thinking. © 2013 Nature Publishing Group

Keyword: Glia; Brain imaging
Link ID: 18610 - Posted: 09.05.2013

By Laura Sanders Rats spent hours in a state of chilly suspended animation after researchers injected a compound into the animals in a cold room. The animals’ heart rates slowed, brain activity became sluggish and body temperature plummeted. The research joins a small number of studies that attempt to induce the metabolically lethargic state known as torpor in animals that can’t normally slow their metabolism. “It’s a breakthrough” in understanding aspects of torpor, says neuroscientist Kelly Drew of the University of Alaska Fairbanks. Lowering the body temperature of a nonhibernating mammal is really hard, says Domenico Tupone of Oregon Health & Science University in Portland. As temperatures inside the body fall, several failsafe systems spring into action. Blood vessels near the skin squeeze tight to hold warmth in, the body starts to shiver and brown fat, a tissue that’s especially plentiful in newborns, starts to produce heat. But Tupone and colleagues bypassed the rats’ defenses against the cold with a compound that’s similar to adenosine, a molecule in the body that signals sleepiness. After about an hour in a room chilled to 15° Celsius, the rats grew lethargic. Their brain waves slowed, their blood pressure dropped and their heart grew sluggish, occasionally skipping beats. The rats’ core temperature dropped from about 38° to about 30° C, or 80° Fahrenheit, the authors report in the Sept. 4 Journal of Neuroscience. Tupone and his colleagues measured even lower temperatures in further experiments — rats’ core body temperature reached 15° C or about 57° F. “That is a pretty amazing temperature. No one has done this before,” he says. © Society for Science & the Public 2000 - 2013

Keyword: Miscellaneous
Link ID: 18609 - Posted: 09.05.2013

Elizabeth Pennisi Dolphins and bats don't have much in common, but they share a superpower: Both hunt their prey by emitting high-pitched sounds and listening for the echoes. Now, a study shows that this ability arose independently in each group of mammals from the same genetic mutations. The work suggests that evolution sometimes arrives at new traits through the same sequence of steps, even in very different animals. The research also implies that this convergent evolution is common—and hidden—within genomes, potentially complicating the task of deciphering some evolutionary relationships between organisms. Nature is full of examples of convergent evolution, wherein very distantly related organisms wind up looking alike or having similar skills and traits: Birds, bats, and insects all have wings, for example. Biologists have assumed that these novelties were devised, on a genetic level, in fundamentally different ways. That was also the case for two kinds of bats and toothed whales, a group that includes dolphins and certain whales, that have converged on a specialized hunting strategy called echolocation. Until recently, biologists had thought that different genes drove each instance of echolocation and that the relevant proteins could change in innumerable ways to take on new functions. But in 2010, Stephen Rossiter, an evolutionary biologist at Queen Mary, University of London, and his colleagues determined that both types of echolocating bats, as well as dolphins, had the same mutations in a particular protein called prestin, which affects the sensitivity of hearing. Looking at other genes known to be involved in hearing, they and other researchers found several others whose proteins were similarly changed in these mammals. © 2012 American Association for the Advancement of Science

Keyword: Hearing; Evolution
Link ID: 18608 - Posted: 09.05.2013

Scientists believe they have discovered a new reason why we need to sleep - it replenishes a type of brain cell. Sleep ramps up the production of cells that go on to make an insulating material known as myelin which protects our brain's circuitry. The findings, so far in mice, could lead to insights about sleep's role in brain repair and growth as well as the disease MS, says the Wisconsin team. The work is in the Journal of Neuroscience. Dr Chiara Cirelli and colleagues from the University of Wisconsin found that the production rate of the myelin making cells, immature oligodendrocytes, doubled as mice slept. The increase was most marked during the type of sleep that is associated with dreaming - REM or rapid eye movement sleep - and was driven by genes. In contrast, the genes involved in cell death and stress responses were turned on when the mice were forced to stay awake. Precisely why we need to sleep has baffled scientists for centuries. It's obvious that we need to sleep to feel rested and for our mind to function well - but the biological processes that go on as we slumber have only started to be uncovered relatively recently. Dr Cirelli said: "For a long time, sleep researchers focused on how the activity of nerve cells differs when animals are awake versus when they are asleep. "Now it is clear that the way other supporting cells in the nervous system operate also changes significantly depending on whether the animal is asleep or awake." The researchers say their findings suggest that sleep loss might aggravate some symptoms of multiple sclerosis (MS), a disease that damages myelin. BBC © 2013

Keyword: Sleep; Glia
Link ID: 18607 - Posted: 09.04.2013

Ed Yong Listen very carefully in the rainforests of Brazil and you might hear a series of quiet, high-pitched squeaks. These are the alarm calls of the black-fronted titi (Callicebus nigrifrons), a monkey with a rusty-brown tail that lives in small family units. The cries are loaded with information. Cristiane Cäsar, a biologist at the University of St Andrews, UK, and her colleagues report that the titis mix and match two distinct calls to tell each other about the type of predator that endangers them, as well as the location of the threat. Her results are published in Biology Letters1. Cäsar's team worked with five groups of titis that live in a private nature reserve in the Minas Gerais region of Brazil. When the researchers placed a stuffed caracara — a bird of prey — in the treetops, the titis gave out A-calls, which have a rising pitch. When the animals saw a ground-based threat — represented by an oncilla, a small spotted cat — they produced B-calls, sounds with a falling pitch. However, when the team moved the predator models around, the monkeys tweaked their calls. If the caracara was on the ground, the monkeys started with at least four A-calls before adding B-calls into the mix. If the oncilla was in a tree, the monkeys made a single introductory A-call before switching to B-calls. “A single call doesn’t really tell the recipient what’s happening, but they can infer the type of predator and its location by listening to the first five or six calls,” says co-author Klaus Zuberbühler of the University of Neuchâtel in Switzerland. “The five different groups were almost unanimous in their response. There was no deviation.” © 2013 Nature Publishing Group

Keyword: Animal Communication; Language
Link ID: 18606 - Posted: 09.04.2013