Chapter 11. Motor Control and Plasticity
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By Meghan Rosen Michael McAlpine’s shiny circuit doesn’t look like something you would stick in your mouth. It’s dashed with gold, has a coiled antenna and is glued to a stiff rectangle. But the antenna flexes, and the rectangle is actually silk, its stiffness melting away under water. And if you paste the device on your tooth, it could keep you healthy. The electronic gizmo is designed to detect dangerous bacteria and send out warning signals, alerting its bearer to microbes slipping past the lips. Recently, McAlpine, of Princeton University, and his colleagues spotted a single E. coli bacterium skittering across the surface of the gadget’s sensor. The sensor also picked out ulcer-causing H. pylori amid the molecular medley of human saliva, the team reported earlier this year in Nature Communications. At about the size of a standard postage stamp, the dental device is still too big to fit comfortably in a human mouth. “We had to use a cow tooth,” McAlpine says, describing test experiments. But his team plans to shrink the gadget so it can nestle against human enamel. McAlpine is convinced that one day, perhaps five to 10 years from now, everyone will wear some sort of electronic device. “It’s not just teeth,” he says. “People are going to be bionic.” McAlpine belongs to a growing pack of tech-savvy scientists figuring out how to merge the rigid, brittle materials of conventional electronics with the soft, curving surfaces of human tissues. Their goal: To create products that have the high performance of silicon wafers — the crystalline material used in computer chips — while still moving with the body. © Society for Science & the Public 2000 - 2012
Link ID: 17455 - Posted: 11.05.2012
By Katherine Harmon With a juicy insect dinner perched on a leaf above the water, what is a hungry little archer fish down below to do? Knock it down with a super-powered, super-precise jet of water that packs six times the power the fish could generate with its own muscles, according to new findings published online October 24 in PLoS ONE. The stunning spitting power of the amazing archer fish (Toxotes jaculatrix) was first described in the 18th century. The creature lives in mostly in mangrove forests and estuaries where insects are prevalent—above water, that is. And these tasty treats are not easily knocked off of the plants that hang over the archer fish’s territory. The insects, such as grasshoppers, can hang on with a force some 10 times their own body weight. So the archer fish has developed an impressive strategy for fetching food that not many other fish can reach. Its water jet can target and dislodge a single insect so that it falls into the water for the fish to eat. Just how the fish manages to do this—and in less than a second—had remained a mystery. Many scientists figured that the source must be a special organ in the fish’s body. “The origin of the effectiveness of the jet squirted by the archer fish has been searched for inside of the fish for nearly 250 years,” Alberto Vailati, a physicist at the University of Milan and co-author of the new paper, said in a prepared statement. © 2012 Scientific American
By ANAHAD O'CONNOR Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Physical exercise not only protected against such age-related brain changes, but also had more of an effect than mentally and socially stimulating activities. In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities. Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the brain’s white matter, which is considered the “wiring” of the brain’s communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and I.Q. As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study and a senior research fellow at Edinburgh. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.” Copyright 2012 The New York Times Company
Link ID: 17427 - Posted: 10.27.2012
by Helen Thomson Paralysis may no longer mean life in a wheelchair. A man who is paralysed from the trunk down has recovered the ability to stand and move his legs unaided thanks to training with an electrical implant. Andrew Meas of Louisville, Kentucky, says it has changed his life (see "I suddenly noticed I can move my pinkie", below). The stimulus provided by the implant is thought to have either strengthened persistent "silent" connections across his damaged spinal cord or even created new ones, allowing him to move even when the implant is switched off. The results are potentially revolutionary, as they indicate that the spinal cord is able to recover its function years after becoming damaged. Previous studies in animals with lower limb paralysis have shown that continuous electrical stimulation of the spinal cord below the area of damage allows an animal to stand and perform locomotion-like movements. That's because the stimulation allows information about proprioception – the perception of body position and muscle effort – to be received from the lower limbs by the spinal cord. The spinal cord, in turn, allows lower limb muscles to react and support the body without any information being received from the brain (Journal of Neuroscience, doi.org/czq67d). Last year, Susan Harkema and Claudia Angeli at the Frazier Rehab Institute and University of Louisville in Kentucky and colleagues tested what had been learned on animals in a man who was paralysed after being hit by a car in 2006. He was diagnosed with a "motor complete" spinal lesion in his neck, which means that no motor activity can be recorded below the lesion. © Copyright Reed Business Information Ltd
Link ID: 17420 - Posted: 10.25.2012
By Michelle Roberts Health editor, BBC News online Exercising in your 70s may stop your brain from shrinking and showing the signs of ageing linked to dementia, say experts from Edinburgh University. Brain scans of 638 people past the age of retirement showed those who were most physically active had less brain shrinkage over a three-year period. Exercise did not have to be strenuous - going for a walk several times a week sufficed, the journal Neurology says. But giving the mind a workout by doing a tricky crossword had little impact. The study found no real brain-size benefit from mentally challenging activities, such as reading a book, or other pastimes such as socialising with friends and family. When the researchers examined the brain's white matter - the wiring that transmits messages round the brain - they found that the people over the age of 70 who were more physically active had fewer damaged areas than those who did little exercise. And they had more grey matter - the parts of the brain where the messages originate. Experts already know that our brains tend to shrink as we age and that this shrinkage is linked to poorer memory and thinking. BBC © 2012
Link ID: 17410 - Posted: 10.23.2012
By Dan Cossins There’s a new suspect in the search for the causes of Parkinson’s disease—deformities in the nuclear membrane of neural stem cells. Scientists observed the same defects, caused by a single gene mutation, in brain tissue samples from deceased Parkinson’s patients, suggesting that nuclear deterioration—and the mutation that drives it—could play a role in the pathology of the disease. The study, published today (October 17) in Nature, also shows that correcting the mutation reverses this phenotype, pointing to new ways to treat this cause of neurodegeneration. “I don’t recall anyone ever suggesting this as a major phenotype [for Parkinson’s], so that’s really quite a big new direction for the field,” said Mark Cookson, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who did not participate in the study. Parkinson’s disease has traditionally been attributed to a loss of dopamine-generating neurons, which leads to the degenerative muscle control that is characteristic of the disease. But Parkinson’s also causes many other sensory problems, which cannot be explained by a dopaminergic mechanism. Over the past 5 years, several groups have shown that disruption of the structure of the nuclear envelope—the lipid bilayer that separates nucleus from cytoplasm—is correlated with aging and certain age-related pathologies in the human brain, though the precise role of nuclear defects in the diseases remained unclear. Meanwhile, since 2004 scientists including Cookson have demonstrated that a mutation in the luceine-rich repeat kinase 2 (LRRK2) gene is correlated with Parkinson’s. However, the molecular and cellular mechanisms by which the LRRK2 mutation might drive disease progression remained a mystery. © 1986-2012 The Scientist
Link ID: 17392 - Posted: 10.20.2012
By Tina Hesman Saey The 2012 Nobel Prize in physiology or medicine was awarded for the discovery that adult cells can be reprogrammed, as scientists did to these neurons, created from skin cells reprogrammed into a type of primordial stem cell and then coaxed into brain cells that control movement.G. Croft and M. Weygandt/The Cell: An Image Library Two scientists who showed that a cell's fate is reversible have won the 2012 Nobel Prize in physiology or medicine. The Nobel committee announced October 8 that John Gurdon and Shinya Yamanaka are being honored for showing that cells once thought to be locked into a specific identity could remember and revert to the supremely flexible state they have in an early embryo. Gurdon’s 1962 work forever changed the view that adult cells are stuck in their fate. In a series of experiments, he transplanted the nucleus — the cellular compartment that contains DNA — from an intestinal cell of an adult frog into a frog egg cell from which the nucleus had been removed. The cell developed into a normal tadpole, demonstrating that DNA contains all the information necessary to make an embryo. More than four decades later, Yamanaka, of Kyoto University in Japan, changed the debate over stem cells when he created induced pluripotent stem cells, which are capable of becoming nearly any cell in the body. He was trying to understand the factors that make stem cells isolated from embryos so malleable; many genes seemed to be involved. Yamanaka used viruses to insert combinations of candidate genes into skin cells, and found that only four genes are required to turn a mouse skin cell into a stem cell. The technique has since been used to convert adult human cells into embryonic-like cells and even to convert skin cells directly into heart or brain cells. © Society for Science & the Public 2000 - 2012
Two pioneers of stem cell research have shared the Nobel prize for medicine or physiology. John Gurdon from the UK and Shinya Yamanaka from Japan were awarded to prize for transforming specialised cells into stem cells.
By ANDREW POLLACK An experimental drug preserved and even improved the walking ability of boys with Duchenne muscular dystrophy in a clinical trial, raising hopes that the first effective treatment for the disease may be on the horizon. Boys with the disease who received the highest dose of the drug had a slightly improved ability to walk after 48 weeks of treatment, the drug’s developer, Sarepta Therapeutics, announced Wednesday. By contrast, the boys who received a placebo suffered a sharp decline in how well they could walk. The drug, called eteplirsen, also appeared to restore levels of the crucial protein that muscular dystrophy patients lack to about half of normal levels, Sarepta said. “I think this changes the entire playing field for muscular dystrophy,” said Dr. Jerry R. Mendell, director of the gene therapy and muscular dystrophy programs at Nationwide Children’s Hospital in Columbus, Ohio, and the lead investigator in the trial. There are many caveats. The trial had only 12 patients, with only four receiving the high dose and four the placebo, and the data has not been reviewed by experts. It is also unclear how long the effects of the drug would last or if safety issues would arise with longer treatment. Also, eteplirsen would be appropriate for only about 13 percent to 15 percent of Duchenne patients, those with the particular genetic mutation the drug is meant to counteract. However, a similar approach might work for some other mutations. © 2012 The New York Times Company
By Gary Stix 14 inSharHuntington’ disease, which killed folk singer Woody Guthrie, seems to put into overdrive the main chemical that turns on brain cells, ultimately leading to their death. The normal function of the neurotransmitter glutamate, the chemical overproduced in Huntington’s, is also intimately involved with learning. Researchers from Ruhr University and the University of Dortmund in Germany have been intrigued by the question of whether the neurodegeneration initiated by glutamate in this genetic disorder is all bad. Is it simply burning out brain circuits? Or might an excess of the chemical also help presymptomatic carriers of the Huntington’s gene or even patients with the disease itself, learn some things faster or better? “Neurotransmission causes cell death but we know from the vast amount of literature that learning processes very much depend on glutamate neurotransmission; so there may be two effects of one and the same process,” says Christian Beste of Ruhr University. “On the one hand this process may lead to neurodegeneration. But on the other hand, it may augment a cognitive process that depends on glutamate transmission.” Beste is the lead author on a paper published this month in Current Biology that found that those who have the genetic mutation for Huntington’s but who have yet to develop inevitable symptoms of the disease perform better on a learning task than a control group that lacks the mutation. The 29 Huntington’s gene carriers learned to detect twice as fast as the 45 controls a change in brightness of a small bar as its orientation on a computer screen altered. In fact, the Huntington’s carriers with the most pronounced mutations—the number of repetitions of a short DNA segment determines how early disease onset occurs—logged the best performance. © 2012 Scientific American,
Link ID: 17311 - Posted: 09.29.2012
By GRETCHEN REYNOLDS Can you improve your body’s ability to remember by making it move? That rather odd-seeming question stimulated researchers at the University of Copenhagen to undertake a reverberant new examination of just how the body creates specific muscle memories and what role, if any, exercise plays in the process. To do so, they first asked a group of young, healthy right-handed men to master a complicated tracking skill on a computer. Sitting before the screen with their right arm on an armrest and a controller similar to a joystick in their right hand, the men watched a red line squiggle across the screen and had to use the controller to trace the same line with a white cursor. Their aim was to remain as close to the red squiggle as possible, a task that required input from both the muscles and the mind. The men repeated the task multiple times, until the motion necessary to track the red line became ingrained, almost automatic. They were creating a short-term muscle memory. The term “muscle memory” is, of course, something of a misnomer. Muscles don’t make or store memories. They respond to signals from the brain, where the actual memories of any particular movement are formed and filed away. But muscle memory — or “motor memory,” as it is more correctly referred to among scientists — exists and can be quite potent. Learn to ride a bicycle as a youngster, abandon the pastime and, 20 years later, you’ll be able to hop on a bicycle and pedal off. Copyright 2012 The New York Times Company
Keyword: Learning & Memory
Link ID: 17304 - Posted: 09.26.2012
by Andy Coghlan Muscles that burn energy without contracting have yielded new clues about how the body retains a constant temperature – and they may provide new targets for combating obesity. Traditionally, the body's main thermostat was thought to be brown fat. It raids the body's white fat stores in cold conditions to burn energy and keep the body warm. Muscles also play a role in keeping the body warm by contracting and triggering the shiver response – but this is only a short-term fix because prolonged shivering damages muscles. Now it seems that muscles have another way to turn up the heat. "Our findings demonstrate for the first time that muscle, which accounts for 40 per cent of body weight in humans, can generate heat independent of shivering," says Muthu Periasamy of Ohio State University in Columbus. Surviving the chill Through experiments on mice that had their usual thermostat – brown fat – surgically removed, Periasamy and his colleagues proved that a protein called sarcolipin helps muscle cells keep the body warm by burning energy, almost like an idling motor car, even if the muscles do not contract. All of the mice had their brown fat removed, but some of them had been genetically engineered to lack sarcolipin too. These rodents could not survive when held at 4 °C, and died of hypothermia within 10 hours. By contrast, mice that could make sarcolipin were able to survive the chilly temperatures and maintained their core body temperature – despite having no brown fat. © Copyright Reed Business Information Ltd.
By Miguel A. L. Nicolelis In 2014 billions of viewers worldwide may remember the opening game of the World Cup in Brazil for more than just the goals scored by the Brazilian national team and the red cards given to its adversary. On that day my laboratory at Duke University, which specializes in developing technologies that allow electrical signals from the brain to control robotic limbs, plans to mark a milestone in overcoming paralysis. If we succeed in meeting still formidable challenges, the first ceremonial kick of the World Cup game may be made by a paralyzed teenager, who, flanked by the two contending soccer teams, will saunter onto the pitch clad in a robotic body suit. This suit—or exoskeleton, as we call it—will envelop the teenager's legs. His or her first steps onto the field will be controlled by motor signals originating in the kicker's brain and transmitted wirelessly to a computer unit the size of a laptop in a backpack carried by our patient. This computer will be responsible for translating electrical brain signals into digital motor commands so that the exoskeleton can first stabilize the kicker's body weight and then induce the robotic legs to begin the back-and-forth coordinated movements of a walk over the manicured grass. Then, on approaching the ball, the kicker will visualize placing a foot in contact with it. Three hundred milliseconds later brain signals will instruct the exoskeleton's robotic foot to hook under the leather sphere, Brazilian style, and boot it aloft. This scientific demonstration of a radically new technology, undertaken with collaborators in Europe and Brazil, will convey to a global audience of billions that brain control of machines has moved from lab demos and futuristic speculation to a new era in which tools capable of bringing mobility to patients incapacitated by injury or disease may become a reality. © 2012 Scientific American
Link ID: 17220 - Posted: 08.30.2012
Helen Shen Automated assistance may soon be available to neuroscientists tackling the brain’s complex circuitry, according to research presented last week at the Aspen Brain Forum in Colorado. Robots that can find and simultaneously record the activity of dozens of neurons in live animals could help researchers to reveal how connected cells interpret signals from one another and transmit information across brain areas — a task that would be impossible using single-neuron studies. The robots are designed to perform whole-cell patch-clamping, a difficult but powerful method that allows neuroscientists to access neurons' internal electrical workings, says Edward Boyden of the Massachusetts Institute of Technology in Cambridge, who is leading the work. Manually performing the method on live animals requires extensive training to perfect and, as a result, only a handful of neurophysiologists use the technique, says Boyden, who presented at the conference. He is developing the automated tool with Craig Forest at the Georgia Institute of Technology in Atlanta and others. “We think that it helps democratize procedures that require a lot of skill,” he says. In May, the group described how a basic version of the robot can record electrical currents in single neurons in the brains of anaesthetized mice1. The robot finds its target on the basis of characteristic changes in the electrical environment near neurons. Then, the device nicks the cell’s membrane and seals itself around the tiny hole to access the neuron's contents. On 24 August, Boyden presented results showing that a more advanced version of the robot could be used to identify and probe four neurons at once — and he says he wants to push the design further, perhaps to tap as many as 100 neurons at a time. © 2012 Nature Publishing Group
Link ID: 17215 - Posted: 08.29.2012
by Jessica Hamzelou When something goes wrong in your brain, you'd think it would be a good idea to get rid of the problem. Turns out, sometimes it's best to keep hold of it. By preventing faulty proteins from being destroyed, researchers have delayed the symptoms of a degenerative brain disorder. SNAP25 is one of three proteins that together make up a complex called SNARE, which plays a vital role in allowing neurons to communicate with each other. In order to work properly, all the proteins must be folded in a specific way. CSP alpha is one of the key proteins that ensures SNAP25 is correctly folded. Cells have a backup system to deal with any misfolded proteins – they are destroyed by a bell-shaped enzyme called a proteasome, which pulls the proteins inside itself and breaks them down. People with a genetic mutation that affects the CSP alpha protein – and its ability to correctly fold SNAP25 – can develop a rare brain disorder called neuronal ceroid lipofuscinosis (NCL). The disorder causes significant damage to neurons – people affected gradually lose their cognitive abilities and struggle to move normally. To find out what role proteasomes might play in NCL, Manu Sharma and his colleagues at Stanford University in California blocked the enzyme in mice that were bred to lack CSP alpha. "We weren't sure what would happen," says Sharma. Either the misfolded SNAP25 would accumulate and harm the cells, or some of the misfolded proteins may work well enough to retain some of their function. © Copyright Reed Business Information Ltd.
By Kathleen Raven A compound already sitting on the shelves of biomedical laboratories and emergency room supply closets seems to interrupt the formation of neurodegenerative protein clumps found in Huntington’s disease, according to a preliminary animal study published August 7 in the Journal of Neuroscience. This versatile agent, called methylene blue, gets a mention in medical literature as early as 1897 and was used to treat, at one time or another, ailments ranging from malaria to cyanide poisoning. The U.S. Food and Drug Administration has never formally approved it as a therapy for any illnesses. But that fact hasn’t stopped biomedical researchers from tinkering with the agent’s apparent ability to improve cognitive function. And although the new paper out today relies on a Huntington’s disease model in flies and mice, scientists are hopeful. "Because of existing knowledge of methylene blue and the fact that it’s not harmful to humans, I would hope that progress toward clinical trials could go relatively quickly," says Leslie Thompson, a neurobiologist at University of California–Irvine and lead author on the new study. Huntington’s disease occurs when the C-A-G sequence of DNA base pairs repeat too often on the HTT gene, resulting in an abnormally long version of the huntingtin protein, that therefore folds incorrectly and forms clumps in the brain. The illness usually begins to affect people in their 30s and 40s, causing movement problems and early death. No drug is currently available to stop the disease from progressing. © 2012 Scientific American
Link ID: 17168 - Posted: 08.15.2012
By KATIE HAFNER SEATTLE — Dr. Richard Wesley has amyotrophic lateral sclerosis, the incurable disease that lays waste to muscles while leaving the mind intact. He lives with the knowledge that an untimely death is chasing him down, but takes solace in knowing that he can decide exactly when, where and how he will die. Under Washington State’s Death With Dignity Act, his physician has given him a prescription for a lethal dose of barbiturates. He would prefer to die naturally, but if dying becomes protracted and difficult, he plans to take the drugs and die peacefully within minutes. “It’s like the definition of pornography,” Dr. Wesley, 67, said at his home here in Seattle, with Mount Rainier in the distance. “I’ll know it’s time to go when I see it.” Washington followed Oregon in allowing terminally ill patients to get a prescription for drugs that will hasten death. Critics of such laws feared that poor people would be pressured to kill themselves because they or their families could not afford end-of-life care. But the demographics of patients who have gotten the prescriptions are surprisingly different than expected, according to data collected by Oregon and Washington through 2011. Dr. Wesley is emblematic of those who have taken advantage of the law. They are overwhelmingly white, well educated and financially comfortable. And they are making the choice not because they are in pain but because they want to have the same control over their deaths that they have had over their lives. © 2012 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 17153 - Posted: 08.13.2012
by Anil Ananthaswamy Advocates of free will can rest easy, for now. A 30-year-old classic experiment that is often used to argue against free will might have been misinterpreted. In the early 1980s, Benjamin Libet, a neuroscientist at the University of California in San Francisco, used electroencephalography (EEG) to record the brain activity of volunteers who had been told to make a spontaneous movement. With the help of a precise timer that the volunteers were asked to read at the moment they became aware of the urge to act, Libet found there was a 200 millisecond delay, on average, between this urge and the movement itself. But the EEG recordings also revealed a signal that appeared in the brain even earlier, 550 milliseconds, on average, before the action. Called the readiness potential, this has been interpreted as a blow to free will, as it suggests that the brain prepares to act well before we are conscious of the urge to move. This conclusion assumes that the readiness potential is the signature of the brain planning and preparing to move. "Even people who have been critical of Libet's work, by and large, haven't challenged that assumption," says Aaron Schurger of the National Institute of Health and Medical Research in Saclay, France. One attempt to do so came in 2009. Judy Trevena and Jeff Miller of the University of Otago in Dunedin, New Zealand, asked volunteers to decide, after hearing a tone, whether or not to tap on a keyboard. The readiness potential was present regardless of their decision, suggesting that it did not represent the brain preparing to move. Exactly what it did mean, though, still wasn't clear. © Copyright Reed Business Information Ltd.
COFFEE can give you the shakes, but caffeine seems to have the opposite effect in people with Parkinson's disease, helping to relieve tremors and get them back on the move. In the past, caffeine has been shown to reduce the risk of Parkinson's, but its effects have never been tested in people who already have the disease. Ronald Postuma of McGill University in Montreal, Canada, and colleagues gave 61 people with Parkinson's a 6-week course of pills containing the caffeine equivalent of about three cups of coffee every day, or a placebo. Only people in the caffeine group showed a significant improvement in tests for motor problems, such as the severity of their tremors, and general mobility (Neurology, DOI: 10.1212/WNL.0b013e318263570d). Motor problems associated with Parkinson's are caused by a lack of dopamine in areas of the brain where dopamine-producing cells are destroyed. Adenosine receptors normally inhibit the production of dopamine. Caffeine blocks adenosine receptors and so acts to boost available dopamine. Drugs that target adenosine receptors are already in clinical trials but caffeine could provide a cheaper alternative. © Copyright Reed Business Information Ltd.
Link ID: 17123 - Posted: 08.04.2012
By Sandra Upson All elite athletes train hard, possess great skills and stay mentally sharp during competition. But what separates a gold medalist from an equally dedicated athlete who comes in 10th place? A small structure deep in the brain may give winners an extra edge. Recent studies indicate that the brain's insular cortex may help a sprinter drive his body forward just a little more efficiently than his competitors. This region may prepare a boxer to better fend off a punch his opponent is beginning to throw as well as assist a diver as she calculates her spinning body's position so she hits the water with barely a splash. The insula, as it is commonly called, may help a marksman retain a sharp focus on the bull's-eye as his finger pulls back on the trigger and help a basketball player at the free-throw line block out the distracting screams and arm-waving of fans seated behind the backboard. The insula does all this by anticipating an athlete's future feelings, according to a new theory. Researchers at the OptiBrain Center, a consortium based at the University of California, San Diego, and the Naval Health Research Center, suggest that an athlete possesses a hyper-attuned insula that can generate strikingly accurate predictions of how the body will feel in the next moment. That model of the body's future condition instructs other brain areas to initiate actions that are more tailored to coming demands than those of also-rans and couch potatoes. This heightened awareness could allow Olympians to activate their muscles more resourcefully to swim faster, run farther and leap higher than mere mortals. In experiments published in 2012, brain scans of elite athletes appeared to differ most dramatically from ordinary subjects in the functioning of their insulas. © 2012 Scientific American
Keyword: Brain imaging
Link ID: 17088 - Posted: 07.25.2012