Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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By Emily Underwood Earlier this month, György Buzsáki of New York University (NYU) in New York City showed a slide that sent a murmur through an audience in the Grand Ballroom of New York’s Midtown Hilton during the annual meeting of the Cognitive Neuroscience Society. It wasn’t just the grisly image of a human cadaver with more than 200 electrodes inserted into its brain that set people whispering; it was what those electrodes detected—or rather, what they failed to detect. When Buzsáki and his colleague, Antal Berényi, of the University of Szeged in Hungary, mimicked an increasingly popular form of brain stimulation by applying alternating electrical current to the outside of the cadaver’s skull, the electrodes inside registered little. Hardly any current entered the brain. On closer study, the pair discovered that up to 90% of the current had been redirected by the skin covering the skull, which acted as a “shunt,” Buzsáki said. For many meeting attendees, the unusual study heightened serious doubts about the mechanism and effectiveness of transcranial direct current stimulation (tDCS), an experimental, noninvasive treatment that uses electrodes to deliver weak current to a person’s forehead, and the related tACS, which uses alternating current. Little is known about how these techniques might influence the brain. Yet many scientific papers have claimed that the techniques can boost mood, alleviate chronic pain, and even make people better at math by directly affecting neuronal activity. This has spawned a cottage industry of do-it-yourself gadgets promising to make people smarter and happier. © 2016 American Association for the Advancement of Science
Link ID: 22126 - Posted: 04.21.2016
Helen Shen Clamping an electrode to the brain cell of a living animal to record its electrical chatter is a task that demands finesse and patience. Known as ‘whole-cell patch-clamping’, it is reputedly the “finest art in neuroscience”, says neurobiologist Edward Boyden, and one that only a few dozen laboratories around the world specialize in. But researchers are trying to demystify this art by turning it into a streamlined, automated technique that any laboratory could attempt, using robotics and downloadable source code. “Patch-clamping provides a unique view into neural circuits, and it’s a very exciting technique but is really underused,” says neuroscientist Karel Svoboda at the Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Virginia. “That’s why automation is a really, really exciting direction.” On 3 March, Boyden, at the Massachusetts Institute of Technology in Cambridge, and his colleagues published detailed instructions on how to assemble and operate an automated system for whole-cell patch-clamping1, a concept that they first described in 20122. The guide represents the latest fruits of Boyden’s partnership with the laboratory of Craig Forest, a mechanical engineer at the Georgia Institute of Technology in Atlanta who specializes in robotic automation for research. © 2016 Nature Publishing Group
Keyword: Brain imaging
Link ID: 22066 - Posted: 04.04.2016
By Ariana Eunjung Cha LAS VEGAS — Jamie Tyler was stressed. He had just endured a half-hour slog through airport security and needed some relief. Many travelers in this situation might have headed for the nearest bar or popped an aspirin. But Tyler grabbed a triangular piece of gadgetry from his bag and held it to his forehead. As he closed his eyes, the device zapped him with low-voltage electrical currents. Within minutes, Tyler said, he was feeling serene enough to face the crowds once again. This is no science fiction. The Harvard-trained neurobiologist was taking advantage of one of his own inventions, a device called Thync, which promises to help users activate their body's “natural state of energy or calm” — for a retail price of a mere $199. Americans’ obsession with wellness is fueling a new category of consumer electronics, one that goes far beyond the ubiquitous Fitbits and UP activity wristbands that only passively monitor users' physical activity. The latest wearable tech, to put it in the simplest terms, is about hacking your brain. These gadgets claim to be able to make you have more willpower, think more creatively and even jump higher. One day, their makers say, the technology may even succeed in delivering on the holy grail of emotions: happiness. There’s real, peer-reviewed science behind the theory driving these devices. It involves stimulating key regions of the brain — with currents or magnetic fields — to affect emotions and physical well-being.
Link ID: 22053 - Posted: 03.31.2016
We might finally be figuring out how an increasingly popular therapy that uses electricity to boost the brain’s functioning has its effects – by pushing up levels of calcium in cells. Transcranial direct current stimulation (tDCS) involves using electrodes to send a weak current across the brain. Stimulating brain tissue like this has been linked to effects ranging from accelerating learning to improving the symptoms of depression and faster recovery from strokes. The broad consensus is that tDCS does this by lowering the threshold at which neurons fire, making it easier for them to pass on electrical signals. This leads to changes in the connectivity between neurons and alters information processing. But the cellular mechanisms that lead to such broad neurological changes are not clear and some researchers suggest that tDCS may not have any effect on the brain. Despite the doubts, devices are being developed for sale to people keen to influence their own brains. Now Hajime Hirase at the RIKEN Brain Science Institute in Tokyo, Japan, and his colleagues may have found an answer. They have identified large, sudden surges in calcium flow in the brains of mice seconds after they receive low doses of tDCS. These surges seem to start in cells called astrocytes – star-shaped cells that don’t fire themselves, but help to strengthen the connections between neurons and regulate the electrical signals that pass between them. © Copyright Reed Business Information Ltd.
Mo Costandi Researchers in the United States have developed a new method for controlling the brain circuits associated with complex animal behaviours, using genetic engineering to create a magnetised protein that activates specific groups of nerve cells from a distance. Understanding how the brain generates behaviour is one of the ultimate goals of neuroscience – and one of its most difficult questions. In recent years, researchers have developed a number of methods that enable them to remotely control specified groups of neurons and to probe the workings of neuronal circuits. The most powerful of these is a method called optogenetics, which enables researchers to switch populations of related neurons on or off on a millisecond-by-millisecond timescale with pulses of laser light. Another recently developed method, called chemogenetics, uses engineered proteins that are activated by designer drugs and can be targeted to specific cell types. Although powerful, both of these methods have drawbacks. Optogenetics is invasive, requiring insertion of optical fibres that deliver the light pulses into the brain and, furthermore, the extent to which the light penetrates the dense brain tissue is severely limited. Chemogenetic approaches overcome both of these limitations, but typically induce biochemical reactions that take several seconds to activate nerve cells. The new technique, developed in Ali Güler’s lab at the University of Virginia in Charlottesville, and described in an advance online publication in the journal Nature Neuroscience, is not only non-invasive, but can also activate neurons rapidly and reversibly. © 2016 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 22034 - Posted: 03.26.2016
By ANDREW POLLACK An experimental drug derived from marijuana has succeeded in reducing epileptic seizures in its first major clinical trial, the product’s developer announced on Monday, a finding that could lend credence to the medical marijuana movement. The developer, GW Pharmaceuticals, said the drug, Epidiolex, achieved the main goal of the trial, reducing convulsive seizures when compared with a placebo in patients with Dravet syndrome, a rare form of epilepsy. GW shares more than doubled on Monday. If Epidiolex wins regulatory approval, it would be the first prescription drug in the United States that is extracted from marijuana. The drug is a liquid containing cannabidiol, a component of marijuana that does not make people high. As many as 30 percent of the nearly 500,000 American children with epilepsy are not sufficiently helped by existing drugs, according to GW. Parents of some of these children have been flocking to try marijuana extracts, prepared by medical marijuana dispensaries. A number of states, in response to pressure from these parents, have passed or considered legislation to make it easier to obtain marijuana-based products. And some families have become “marijuana refugees,” moving to Colorado where it has been easier to obtain a particular extract, known as Charlotte’s Web, after the girl who first used it to control seizures. Hundreds of other children and young adults have been using Epidiolex outside of clinical trials, under programs that allow desperate patients to use experimental drugs. While many parents have reported significant reductions in seizures, experts have been cautious about anecdotal reports, saying that such treatments needed to be compared with a placebo to make sure they work. As such, the results from the GW trial have been closely watched. © 2016 The New York Times Company
By Sandra G. Boodman Kim Pace was afraid he was dying. In six months he had lost more than 30 pounds because a terrible stabbing sensation on the left side of his face made eating or drinking too painful. Brushing his teeth was out of the question and even the slightest touch triggered waves of agony and a shocklike pain he imagined was comparable to electrocution. Painkillers, even morphine, brought little relief. Unable to work and on medical leave from his job as a financial consultant for a bank, Pace, then 59, had spent the first half of 2012 bouncing among specialists in his home state of Pennsylvania, searching for help from doctors who disagreed about the nature of his illness. Some thought his searing pain might be the side effect of a drug he was taking. Others suspected migraines, a dental problem, mental illness, or an attempt to obtain painkillers. Even after a junior doctor made what turned out to be the correct diagnosis, there was disagreement among specialists about its accuracy or how to treat Pace. His wife, Carol, a nurse, said she suspects that the couple’s persistence and propensity to ask questions led her husband to be branded “a difficult case” — the kind of patient whom some doctors avoid. And on top of that, a serious but entirely unrelated disorder further muddied the diagnostic picture. So on July 17, 2012, when Pace told his wife he thought he was dying, she fired off an emotional plea for help to the office of a prominent specialist in Baltimore. “I looked at Kim and it hit me: He was going to die,” she said. “He was losing weight and his color was ashen” and doctors were “blowing him off. I thought, ‘Okay, that’s it,’ and the nurse in me took over.”
By Simon Makin Brain implants have been around for decades—stimulating motor areas to alleviate Parkinson's disease symptoms, for example—but until now they have all suffered from the same limitation: because brains move slightly during physical activity and as we breathe and our heart beats, rigid implants rub and damage tissue. This means that eventually, because of both movement and scar-tissue formation, they lose contact with the cells they were monitoring. Now a group of researchers, led by chemist Charles Lieber of Harvard University, has overcome these problems using a fine, flexible mesh. In 2012 the team showed that cells could be grown around such a mesh, but that left the problem of how to get one inside a living brain. The solution the scientists devised was to draw the mesh—measuring a few millimeters wide—into a syringe, so it would roll up like a scroll inside the 100-micron-wide needle, and inject it through a hole in the skull. In a study published in Nature Nanotechnology last year, the team injected meshes studded with 16 electrodes into two brain regions in mice. The mesh is composed of extremely thin, nanoscale polymer threads, sparsely distributed so that 95 percent of it is empty space. It has a level of flexibility similar to brain tissue. “You're starting to make this nonliving system look like the biological system you're trying to probe,” Lieber explains. “That's been the goal of my group's work, to blur the distinction between electronics as we know it and the computer inside our heads.” © 2016 Scientific American
Keyword: Brain imaging
Link ID: 21950 - Posted: 03.03.2016
By Sheena Goodyear, A brain implant the size of a paper-clip might one day help paralyzed people regain the ability to use their arms and legs via a wireless connection that will transmit their thoughts to an exoskeleton. It's not the first technology to allow paralyzed people to operate mechanical limbs with signals from their brain, but it has the potential to revolutionize the field because it's minimally invasive and totally wireless. It's made possible because of a matchstick-sized implant called a stentrode, crafted from nitinol, an alloy that is commonly used in brassiere underwires and eyeglass frames, according to a study published in the journal Nature Biotechnology. "It's really a new method for getting brain data out of the brain without performing brain surgery," Thomas Oxley, a neurologist at the University of Melbourne who designed the device, told CBC News. "Part of the reason that brain-machine interfaces have not been successful to this point is because they get rejected by the body, and the reason they get rejected is because they all require direct implantation into the brain. And to do that you have to take off the skull — you have to perform a craniotomy." ©2016 CBC/Radio-Canada.
Link ID: 21886 - Posted: 02.11.2016
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,
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
Fergus Walsh Medical correspondent UK doctors in Sheffield say patients with multiple sclerosis (MS) are showing "remarkable" improvements after receiving a treatment usually used for cancer. About 20 patients have received bone marrow transplants using their own stem cells. Some patients who were paralysed have been able to walk again. Prof Basil Sharrack, of Sheffield's Royal Hallamshire Hospital, said: "To have a treatment which can potentially reverse disability is really a major achievement." Around 100,000 people in the UK have MS, an incurable neurological condition. Most patients are diagnosed in their 20s and 30s. The disease causes the immune system to attack the lining of nerves in the brain and spinal cord. The treatment - known as an autologous haematopoietic stem cell transplant (HSCT) - aims to destroy the faulty immune system using chemotherapy. It is then rebuilt with stem cells harvested from the patient's own blood. These cells are at such an early stage they've not developed the flaws that trigger MS. Prof John Snowden, consultant haematologist at Royal Hallamshire Hospital, said: "The immune system is being reset or rebooted back to a time point before it caused MS." About 20 MS patients have been treated in Sheffield in the past three years. Prof Snowden added: "It's clear we have made a big impact on patients' lives, which is gratifying." In MS the protective layer surrounding nerve fibres in the brain and spinal cord - known as myelin - becomes damaged. The immune system mistakenly attacks the myelin, causing scarring or sclerosis. © 2016 BBC.
By Stephani Sutherland A technique called optogenetics has transformed neuroscience during the past 10 years by allowing researchers to turn specific neurons on and off in experimental animals. By flipping these neural switches, it has provided clues about which brain pathways are involved in diseases like depression and obsessive-compulsive disorder. “Optogenetics is not just a flash in the pan,” says neuroscientist Robert Gereau of Washington University in Saint Louis. “It allows us to do experiments that were not doable before. This is a true game changer like few other techniques in science.” Since the first papers were published on optogenetics in the mid-aughts some researchers have mused about one day using optogenetics in patients, imagining the possibility of an off-switch for depression, for instance. The technique, however, would require that a patient submit to a set of highly invasive medical procedures: genetic engineering of neurons to insert molecular switches to activate or switch off cells, along with threading of an optical fiber into the brain to flip those switches. Spurred on by a set of technical advances, optogenetics pioneer Karl Deisseroth, together with other Stanford University researchers, has formed a company to pursue optogenetics trials in patients within the next several years—one of several start-ups that are now contemplating clinical trials of the technique. Circuit Therapeutics, founded in 2010, is moving forward with specific plans to treat neurological diseases. (It also partners with pharmaceutical companies to help them use optogenetics in animal research to develop novel drug targets for human diseases.) © 2016 Scientific America
Keyword: Pain & Touch
Link ID: 21758 - Posted: 01.07.2016
By Diana Kwon Symptoms come and go in most cases of multiple sclerosis (MS), a chronic disease in which the immune system attacks myelin, the nonconductive sheath that surrounds neurons' axons. Yet 10 to 15 percent of cases are progressive rather than relapsing. This more severe version appears later in life and is marked by steadily worsening symptoms. No treatments are currently available, but that might be about to change. In September pharmaceutical company Hoffmann–La Roche announced positive results from three large clinical trials of ocrelizumab, an injectable antibody medication that targets B cells, for both relapsing and progressive MS. They found that the drug was more effective at treating relapsing MS than interferon beta-1a (Rebif), a top-performing drug now used to treat the disease. Even more exciting, it slowed the advance of symptoms in patients with progressive MS for the entire 12-week duration of the study. “The drug has dramatic effects on relapsing MS, and we finally have our foot in the door with the progressive form,” says Stephen Hauser, a neurologist at the University of California, San Francisco, who was involved in the trials. The fact that ocrelizumab works on both types of MS is a tantalizing clue for scientists trying to understand the root causes of the disease and figure out why the inflammation of the relapsing form eventually turns into progressive degeneration in some patients. “These results give evidence that the inflammatory and the degenerative components of MS are related,” Hauser says. “The big question now is, If we begin treatment really early, can we protect relapsing patients from developing the progressive problems later on?” © 2015 Scientific American
Keyword: Multiple Sclerosis
Link ID: 21724 - Posted: 12.27.2015
When anticonvulsant drugs fail to control epilepsy, surgery can be used as a last resort: removing the part of the brain thought to be the source of someone’s seizures. Unfortunately, this doesn’t always work. A computer model of brain activity could change things for the better by allowing surgeons to more precisely tailor the procedure to the individual. Seizures are caused by sudden surges in electrical activity in the brain. EEG scans made during a seizure can capture what is going on, providing a clue to the part of the brain that needs to be cut out. Even so, the surgery still fails to prevent seizures in 30 per cent of cases. There are other ways to track down the source of someone’s seizures, however. For example, the connectivity of the brain’s neurons and the surface area of affected regions is different in people with epilepsy compared with those who do not have the condition. Frances Hutchings at Newcastle University, UK and her colleagues have shown that these differences can be picked up using a combination of fMRI scans and diffusion tensor imaging (DTI). They used this data to model the brains of 22 people with epilepsy. By simulating the brain’s electrical activity, they were able to see where it went awry and identify the region where seizures were most likely to originate in each individual. © Copyright Reed Business Information Ltd.
Sara Reardon Manipulating brain circuits with light and drugs can cause ripple effects that could muddy experimental results. In the tightly woven networks of the brain, tugging one neuronal thread can unravel numerous circuits. Because of that, the authors of a paper1 published in Nature on 9 December caution that techniques such as optogenetics — activating neurons with light to control brain circuits — and manipulation with drugs could lead researchers to jump to unwarranted conclusions. In work with rats and zebra finches, neuroscientist Bence Ölveczky of Harvard University in Cambridge, Massachusetts, and his team found that stimulating one part of the brain to induce certain behaviours might cause other, unrelated parts to fire simultaneously, and so make it seem as if these circuits are also involved in the behaviour. According to Ölveczky, the experiments suggest that although techniques such as optogenetics may show that a circuit can perform a function, they do not necessarily show that it normally performs that function. “I don’t want to say other studies have been wrong, but there is a danger to overinterpreting,” he says. Ölveczky and his colleagues discovered these discrepancies by chance while studying rats that they had trained to press a lever in a certain pattern. They injected a drug called muscimol, which temporarilty shuts off neurons, into a part of the motor cortex that is involved in paw movement. The animals were no longer able to perform the task, which might be taken as evidence that neurons in this brain region were necessary to its performance. © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 21690 - Posted: 12.10.2015
Angus Chen Parents of children with severe epilepsy have reported incredible recoveries when their children were given cannabidiol, a derivative of marijuana. The drug, a non-psychoactive compound that occurs naturally in cannabis, has been marketed with epithets like Charlotte's Web and Haleigh's Hope. But those parents were taking a risk; there has been no clinical data on cannabidiol's safety of efficacy as an anti-epileptic. This week, doctors are presenting the first studies trying to figure out if cannabidiol actually works. They say the studies' results are promising, but with a grain of salt. The largest study being presented at the American Epilepsy Society meeting in Philadelphia this week was started in 2014 with 313 children from 16 different epilepsy centers around the country. Over the course of the three-month trial, 16 percent of the participants withdrew because the cannabidiol was either ineffective or had adverse side-effects, says Dr. Orrin Devinsky, a neurologist at the New York University Langone Medical Center and lead author on the study. But for the 261 patients that continued taking cannabidiol, the number of convulsive seizures, called grand mal or tonic-clonic seizures, went down by about half on average. Devinsky says that some children continued to experience benefits on cannabidiol after the trial ended. "In the subsequent periods, which are very encouraging, 9 percent of all patients and 13 percent of those with Dravet Syndrome epilepsy were seizure-free. Many have never been seizure-free before," he says. It's one of several [at least four. checking] papers on cannabidiol being presented this week at the American Epilepsy Society meeting in Philadelphia. © 2015 npr
A woman born incapable of feeling pain has been hurt for the first time – thanks to a drug normally prescribed for opioid overdoses. She was burned with a laser, and quite liked the experience. The breakthrough may lead to powerful new ways to treat painful conditions such as arthritis. Only a handful people around the world are born unable to feel pain. These individuals can often suffer a range of injuries when they are young. Babies with the condition tend to chew their fingers, toes and lips until they bleed, and toddlers can suffer an increased range of knocks, tumbles and encounters with sharp or hot objects. The disorder is caused by a rare genetic mutation that results in a lack of ion channels that transport sodium across sensory nerves. Without these channels, known as Nav1.7 channels, nerve cells are unable to communicate pain. Researchers quickly sought to make compounds that blocked Nav1.7 channels, thinking they might be able to block pain in people without the disorder. “It looked like a fantastic drug target,” says John Wood at University College London. “Pharma companies went bananas and made lots of drugs.” But while a few compounds saw some success, none brought about the total pain loss seen in people who lack the channel naturally. © Copyright Reed Business Information Ltd.
Laura Sanders Taking a pregnancy hormone staves off multiple sclerosis relapses, a small clinical trial suggests. The results hint at a potential therapy for women who suffer from MS, a debilitating disease in which the body’s immune system attacks the insulation that wraps around nerve cell fibers. A curious observation kicked off this line of research: Pregnancy offers a temporary reprieve for women with MS. Since that discovery, in the 1990s, scientists have been testing whether certain pregnancy hormones might combat MS in women who aren’t pregnant. In addition to a standard MS drug, 164 women with MS received either a placebo or estriol, an estrogen made by the placenta that peaks toward the end of pregnancy. After two years, women who received estriol had an average of 0.25 relapses a year, while women who received the placebo had 0.37 relapses a year, UCLA neurologist Rhonda Voskuhl and colleagues write online November 24 in Lancet Neurology. Researchers don’t know whether estriol would have similar effects in men with MS. The results warrant a larger clinical trial, the authors say. An accompanying commentary in the same issue of Lancet Neurology questions the results, though. MS specialist Annette Langer-Gould of Kaiser Permanente in Pasadena, Calif., raises methodological issues and writes that pregnancy comes with a host of changes that could be responsible for protection from MS. © Society for Science & the Public 2000 - 2015.
By Seth Fletcher To solve the mysteries of the brain, scientists need to delicately, precisely monitor neurons in living subjects. Brain probes, however, have generally been brute-force instruments. A team at Harvard University led by chemist Charles Lieber hopes that silky soft polymer mesh implants will change this situation. So far the researchers have tested the mesh, which is embedded with electronic sensors, in living mice. Once it has been proved safe, it could be used in people to study how cognition arises from the action of individual neurons and to treat diseases such as Parkinson's. © 2015 Scientific American
Keyword: Brain imaging
Link ID: 21645 - Posted: 11.20.2015