Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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Combining the estrogen hormone estriol with Copaxone, a drug indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS), may improve symptoms in patients with the disorder, according to preliminary results from a clinical study of 158 patients with relapsing remitting multiple sclerosis (RRMS). The findings were presented today by Rhonda Voskuhl, M.D., from the University of California, Los Angeles, at the American Academy of Neurology Annual Meeting in Philadelphia. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health; and the National Multiple Sclerosis Society. “While these results are encouraging, the results of this Phase II study should be considered preliminary as a larger study would be needed to know whether benefits outweigh the risks for persons affected by MS. At present, we cannot recommend estrogen as part of standard therapy for MS. We encourage patients to talk with their doctors before making any changes to their treatment plans,” said Walter Koroshetz, M.D., deputy director of NINDS. MS is an autoimmune disorder in which immune cells break down myelin, a protective covering that wraps around nerve cells. Loss of myelin results in pain, movement and balance problems as well as changes in cognitive ability. RRMS is the most common form of the disorder. Patients with RRMS experience relapses, or flare-ups, of neurological symptoms, followed by recovery periods during which the symptoms improve.
Scientists have bioengineered, in neurons cultured from rats, an enhancement to a cutting edge technology that provides instant control over brain circuit activity with a flash of light. The research funded by the National Institutes of Health adds the same level of control over turning neurons off that, until now, had been limited to turning them on. “What had been working through a weak pump can now work through a highly responsive channel with many orders of magnitude more impact on cell function,” explained Karl Deisseroth, M.D., Ph.D., It is like going from a squirt to a gushing hose. Deisseroth and colleagues report on what is being hailed as a marvel of genetic engineering in the April 25, 2014 issue of the journal Science. Deisseroth’s team had pioneered the use of light pulses to control brain circuitry in animals genetically engineered to be light-responsive — optogenetics. Genes that allow the sun to control light-sensitive primitive organisms like algae, melded with genes that make fluorescent marker proteins, are fused with a deactivated virus that delivers them to specific types of neurons which they become part of — allowing pulses of light to similarly commandeer brain cells.
Keyword: Brain imaging
Link ID: 19537 - Posted: 04.26.2014
By JAMES GORMAN SAN DIEGO — Dr. Karl Deisseroth is having a very early breakfast before the day gets going at the annual meeting of the Society for Neuroscience. Thirty thousand people who study the brain are here at the Convention Center, a small city’s worth of badge-wearing, networking, lecture-attending scientists. For Dr. Deisseroth, though, this crowd is a bit like the gang at Cheers — everybody knows his name. He is a Stanford psychiatrist and a neuroscientist, and one of the people most responsible for the development of optogenetics, a technique that allows researchers to turn brain cells on and off with a combination of genetic manipulation and pulses of light. He is also one of the developers of a new way to turn brains transparent, though he was away when some new twists on the technique were presented by his lab a day or two earlier. “I had to fly home to take care of the kids,” he explained. He went home to Palo Alto to be with his four children, while his wife, Michelle Monje, a neurologist at Stanford, flew to the conference for a presentation from her lab. Now she was home and, here he was, back at the conference, looking a bit weary, eating eggs, sunny side up, and talking about the development of new technologies in science. A year ago, President Obama announced an initiative to invest in new research to map brain activity, allocating $100 million for the first year. The money is a drop in the bucket compared with the $4.5 billion the National Institutes of Health spends annually on neuroscience, but it is intended to push the development of new techniques to investigate the brain and map its pathways, starting with the brains of small creatures like flies. Cori Bargmann of Rockefeller University, who is a leader of a committee at the National Institutes of Health setting priorities for its piece of the brain initiative, said optogenetics was a great example of how technology could foster scientific progress. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19520 - Posted: 04.22.2014
by Ashley Yeager A nerve cell's long, slender tentacle isn’t evenly coated with an insulating sheath as scientists had thought. Instead, many nerve cells in the brains of mice have stretches of these tentacles, called axons, that are naked, researchers report April 18 in Science. The unsheathed feeler can be as long as 80 micrometers. Nerve cells can also have specific patterns in the gaps of the insulating layer, called myelin. The differences in the thickness of that coating may control how fast signals travel between nerve cells, the scientists suggest. The finding could have implications for understanding nerve-based diseases, such as multiple sclerosis, and improve scientists’ understanding of how signals are transmitted in the brain. © Society for Science & the Public 2000 - 2013.
Everything we do — all of our movements, thoughts and feelings – are the result of neurons talking with one another, and recent studies have suggested that some of the conversations might not be all that private. Brain cells known as astrocytes may be listening in on, or even participating in, some of those discussions. But a new mouse study suggests that astrocytes might only be tuning in part of the time — specifically, when the neurons get really excited about something. This research, published in Neuron, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For a long time, researchers thought that the star-shaped astrocytes (the name comes from the Greek word for star) were simply support cells for the neurons. It turns out that these cells have a number of important jobs, including providing nutrients and signaling molecules to neurons, regulating blood flow, and removing brain chemicals called neurotransmitters from the synapse. The synapse is the point of information transfer between two neurons. At this connection point, neurotransmitters are released from one neuron to affect the electrical properties of the other. Long arms of astrocytes are located next to synapses, where they can keep tabs on the conversations going on between neurons. In recent years, it has been shown that astrocytes may also play a role in neuronal communication. When neurons release neurotransmitters, levels of calcium change within astrocytes. Calcium is critical for many processes, including release of molecules from the cell, and activation of a host of proteins within the cell. The role of this astrocytic calcium signaling for brain function remains a mystery.
Link ID: 19505 - Posted: 04.17.2014
By CATHERINE SAINT LOUIS ALEXANDRIA, N.H. — For most of his life, Kevin Ramsey has lived with epileptic seizures that drugs cannot control. At least once a month, he would collapse, unconscious and shaking violently, sometimes injuring himself. Nighttime seizures left him exhausted at dawn, his tongue a bloody mess. After episodes at work, he struggled to stay employed. Driving became too risky. At 28, he sold his truck and moved into his mother’s spare bedroom. Cases of intractable epilepsy rarely have happy endings, but today Mr. Ramsey is seizure-free. A novel battery-powered device implanted in his skull, its wires threaded into his brain, tracks its electrical activity and quells impending seizures. At night, he holds a sort of wand to his head and downloads brain data from the device to a laptop for his doctors to review. “I’m still having seizures on the inside, but my stimulator is stopping all of them,” said Mr. Ramsey, 36, whose hands shake because of one of the three anti-seizure drugs he still must take. “I can do things on my own I couldn’t do before. I can go to the store on my own, and get my groceries. Before, I wouldn’t have been able to drive.” Just approved by the Food and Drug Administration, the long-awaited device, called the RNS System, aims to reduce seizures and to improve the lives of an estimated 400,000 Americans whose epilepsy cannot be treated with drugs or brain surgery. “This is the first in what I believe is a new generation of therapy for epilepsy,” said Dr. Dileep R. Nair, head of adult epilepsy at the Cleveland Clinic and an investigator in the pivotal trial for NeuroPace’s RNS. “It’s delivering local therapy. It’s not taking tissue out; the brain is left intact. And it’s unlike a drug, which is a shotgun approach.” © 2014 The New York Times Company
Link ID: 19407 - Posted: 03.25.2014
By Maggie Fox Medical marijuana pills or an oral spray made from cannabis may help ease some of the painful spasms caused by multiple sclerosis that make day-to-day life hard for patients, according to new guidelines from the American Academy of Neurology. But the synthetic formulations of marijuana don’t change the course of the disease and might cause unpleasant side-effects, the experts at the academy caution. There is not enough evidence to make any recommendation on smoking marijuana for MS patients, stresses Dr. Vijayshree Yadav of Oregon Health & Science University, who led the team writing the guidelines. Synthetic marijuana in pill form, including the Marinol brand, is legal for use in treating nausea and loss of appetite in cancer. An oral spray called Sativex is approved for treating MS symptoms in Britain but not in the U.S. MS patients often seek alternative and complementary therapies because they have so few options for the chronic and incurable condition, caused when the immune system mistakenly attacks the nerves. A review of those therapies found there's no evidence most of them work. The review found that the herb Ginkgo biloba might help fatigue, but not thinking and memory problems. There’s also some evidence that magnetic therapy may help fatigue.
Keyword: Multiple Sclerosis
Link ID: 19402 - Posted: 03.25.2014
By Michelle Roberts Health editor, BBC News online Statins may be useful in treating advanced multiple sclerosis (MS), say UK researchers. Early trial results in The Lancet show the cholesterol-lowering pills slow brain shrinkage in people with MS. The University College London (UCL) scientists say large trials can now begin. These will check whether statins benefit MS patients by slowing progression of the disease and easing their symptoms. MS is a major cause of disability, affecting nerves in the brain and spinal cord, which causes problems with muscle movement, balance and vision. Currently there is no cure, although there are treatments that can help in the early stages of the disease. Usually, after around 10 years, around half of people with MS will go on to develop more advanced disease - known as secondary progressive MS. It is this later stage disease that Dr Jeremy Chataway and colleagues at UCL hope to treat with low cost statins. To date, no licensed drugs have shown a convincing impact on this later stage of the disease. For their phase two trial, which is published in the Lancet, Dr Chataway's team randomly assigned 140 people with secondary progressive MS to receive either 80mg of a statin called simvastatin or a placebo for two years. The high, daily dose of simvastatin was well tolerated and slowed brain shrinkage by 43% over two years compared with the placebo. Dr Chataway said: "Caution should be taken regarding over-interpretation of our brain imaging findings, because these might not necessarily translate into clinical benefit. However, our promising results warrant further investigation in larger phase three disability-driven trials." BBC © 2014
Keyword: Multiple Sclerosis
Link ID: 19383 - Posted: 03.19.2014
By Klint Finley Today’s neuroscientists need expertise in more than just the human brain. They must also be accomplished hardware engineers, capable of building new tools for analyzing the brain and collecting data from it. There are many off-the-shelf commercial instruments that help you do such things, but they’re usually expensive and hard to customize, says Josh Siegle, a doctoral student at the Wilson Lab at MIT. “Neuroscience tends to have a pretty hacker-oriented culture,” he says. “A lot of people have a very specific idea of how an experiment needs to be done, so they build their own tools.” The problem, Siegle says, is that few neuroscientists share the tools they build. And because they’re so focused on creating tools for their specific experiments, he says, researchers don’t often consider design principles like modularity, which would allow them to reuse tools in other experiments. That can mean too much redundant work as researchers spend time solving problems others already have solved, and building things from scratch instead of repurposing old tools. ‘We just want to build awareness of how open source eliminates redundancy, reduces costs, and increases productivity’ That’s why Siegle and Jakob Voigts of the Moore Lab at Brown University founded Open Ephys, a project for sharing open source neuroscience hardware designs. They started by posting designs for the tools they use to record electrical signals in the brain. They hope to kick start an open source movement within neuroscience by making their designs public, and encouraging others to do the same. “We don’t necessarily want people to use our tools specifically,” Siegle says. “We just want to build awareness of how open source eliminates redundancy, reduces costs, and increase productivity.” © 2014 Condé Nast.
Link ID: 19353 - Posted: 03.12.2014
by Nathan Seppa MS patients who harbor low levels of vitamin D early in their disease fare worse over the next several years than patients with higher levels. Multiple sclerosis is marked by damage to the fatty sheaths coating nerve fibers in the brain. The result can be an off-and-on series of symptoms including loss of muscle control, numbness and problems thinking. Vitamin D, which the body makes from sun exposure, has shown promise in fighting a variety of diseases and may limit this MS onslaught (SN: 7/16/11, p. 22). In 2002, researchers studying the effect of the drug beta-interferon-1b against MS set aside blood samples from 465 patients. When researchers recently analyzed those samples, they found that patients who had blood levels of vitamin D exceeding 20 nanograms per milliliter at six and 12 months after the onset of MS had fewer symptom flare-ups during the rest of the five-year study than those with lower readings did. Some scientists think 20 nanograms per milliliter is a healthy level; others see 30 as a healthier minimum. MRI scans revealed that, after five years, those who had started out with low vitamin D levels had four times as much myelin damage as those who had higher levels. The results appear in the March JAMA Neurology. A. Ascherio et al. Vitamin D as an early predictor of multiple sclerosis activity and progression. JAMA Neurology. Vol. 71, March 2014, p. 306. doi:10.1001/jamaneurol.2013.5993. © Society for Science & the Public 2000 - 2013
By Debra Weiner An active lifestyle improves brain health, scientists have long believed. The studies bear this out: physical, intellectual and social activity—or “environmental enrichment,” in the parlance—enhances learning and memory and protects against aging and neurological disease. Recent research suggests one benefit of environmental enrichment at the cellular level: it repairs brain myelin, the protective insulation surrounding axons, or nerve fibers, which can be lost because of aging, injury or diseases such as multiple sclerosis. But how does an enriched environment trigger myelin repair in the first place? The answer appears to involve naturally occurring membrane-wrapped packets called exosomes. A number of different cell types release these little sacs of proteins and genetic material into the body's fluids. Loaded with signaling molecules, exosomes spread through the body “like messages in a bottle,” says R. Douglas Fields, a neurobiologist at the National Institutes of Health. They target particular cells and change their behavior. In animal studies, exosomes secreted by immune cells during environmental enrichment caused cells in the brain to start myelin repair. Researchers think exosomes might find use as biomarkers for diagnosing diseases or as vehicles to deliver cancer drugs or other therapeutic agents. The exosomes produced during environmental enrichment carry microRNAs—small pieces of genetic material—which appear to instruct immature cells in the brain to develop into myelin-making cells called oligodendrocytes. When researchers at the University of Chicago withdrew exosomes from the blood of rats and administered them to aging animals, the older rats' myelin levels rose by 62 percent, the team reported in February in Glia. © 2014 Scientific American
By Ariana Eunjung Cha, Standing in a Wisconsin State Capitol hearing room surrounded by parents hugging their seriously ill children, Sally Schaeffer began to cry as she talked about her daughter. Born with a rare chromosomal disorder, 6-year-old Lydia suffers from life-threatening seizures that doctors haven’t been able to control despite countless medications. The family’s last hope: medical marijuana. Schaeffer, 39, didn’t just ask lawmakers to legalize the drug. She begged. “If it was your child and you didn’t have options, what would you do?” she said during her testimony in Madison on Feb. 12. The representatives were so moved that they introduced a bipartisan bill to allow parents in situations similar to Schaeffer’s to use the drug on their children. Emboldened by stories circulated through Facebook, Twitter and the news media about children with seizure disorders who have been successfully treated with a special oil extract made from cannabis plants, mothers have become the new face of the medical marijuana movement. Similar scenes have been playing out in recent weeks in other states where medical marijuana remains illegal: Oklahoma, Florida, Georgia, Utah, New York, North Carolina, Alabama, Kentucky. The “mommy lobby” has been successful at opening the doors to legalizing marijuana — if only a crack, in some places — where others have failed. In the 1970s and ’80s, mothers were on the other side of the issue, successfully fending off efforts to decriminalize marijuana with heartbreaking stories about how their teenage children’s lives unraveled when they began to use the drug. © 1996-2014 The Washington Post
By NICHOLAS RICCARDI, Associated Press COLORADO SPRINGS, Colo. (AP) — The doctors were out of ideas to help 5-year-old Charlotte Figi. Suffering from a rare genetic disorder, she had as many as 300 grand mal seizures a week, used a wheelchair, went into repeated cardiac arrest and could barely speak. As a last resort, her mother began calling medical marijuana shops. Two years later, Charlotte is largely seizure-free and able to walk, talk and feed herself after taking oil infused with a special pot strain. Her recovery has inspired both a name for the strain of marijuana she takes that is bred not to make users high — Charlotte's Web — and an influx of families with seizure-stricken children to Colorado from states that ban the drug. "She can walk, talk; she ate chili in the car," her mother, Paige Figi, said as her dark-haired daughter strolled through a cavernous greenhouse full of marijuana plants that will later be broken down into their anti-seizure components and mixed with olive oil so patients can consume them. "So I'll fight for whomever wants this." Doctors warn there is no proof that Charlotte's Web is effective, or even safe. In the frenzy to find the drug, there have been reports of non-authorized suppliers offering bogus strains of Charlotte's Web. In one case, a doctor said, parents were told they could replicate the strain by cooking marijuana in butter. Their child went into heavy seizures. "We don't have any peer-reviewed, published literature to support it," Dr. Larry Wolk, the state health department's chief medical officer, said of Charlotte's Web. Still, more than 100 families have relocated since Charlotte's story first began spreading last summer, according to Figi and her husband. The relocated families have formed a close-knit group in Colorado Springs, the law-and-order town where the dispensary selling the drug is located. They meet for lunch, support sessions and hikes. © 2014 Hearst Communications, Inc.
By CATHERINE SAINT LOUIS Does chocolate really hurt dogs? It can, depending on their weight and how much they eat, so be vigilant this Valentine’s Day. Stimulants in chocolate can lead to vomiting, diarrhea, agitation and life-threatening elevated heart rates or seizures. “Dogs have no off button,” said Dr. Tina Wismer, the medical director of the ASPCA Animal Poison Control Center. “If you or I ate 10 percent of our body weight in chocolate, we’d have the same problems. A 10-pound dog can easily eat a pound of chocolate.” The darker the chocolate, the more toxic it is. For a 20-pound dog, 9 ounces of milk chocolate can cause seizures, but it takes only 1.5 ounces of baker’s chocolate, she said. Signs of chocolate poisoning usually appear six to 12 hours after ingestion, according to The Merck Veterinary Manual. “Seizures due to toxicity don’t stop unless you treat them,” Dr. Wismer said. So head to the emergency clinic or veterinarian if you come home to find your dog vomiting repeatedly and extremely agitated, and certainly if the pet is unconscious and its limbs are shaking. By contrast, dogs who vomit once and fall sleep can be watched at home, she said. Unlike cats, dogs like sweets. So it’s best to keep chocolate stored away and off countertops, which are no match for a motivated climber. © 2014 The New York Times Company
A food poisoning bacterium may be implicated in MS, say US researchers. Lab tests in mice by the team from Weill Cornell Medical College revealed a toxin made by a rare strain of Clostridium perfringens caused MS-like damage in the brain. And earlier work by the same team, published in PLoS ONE, identified the toxin-producing strain of C. perfringens in a young woman with MS. But experts urge caution, saying more work is needed to explore the link. No-one knows the exact cause of Multiple sclerosis (MS), but it is likely that a mixture of genetic and environmental factors play a role. It's a neurological condition which affects around 100,000 people in the UK. Most cases of human infection occur as food poisoning - diarrhoea and stomach cramps that usually resolve within a day or so. More rarely, the bacterium can cause gas gangrene. And a particular strain of C. perfringens, Type B, which the Weill team says it identified in a human for the first time, makes a toxin that can travel through blood to the brain. In their lab studies on rodents the researchers found that the toxin, called epsilon, crossed the blood-brain barrier and killed myelin-producing cells - the typical damage seen in MS. BBC © 2014
By Deborah Kotz / Globe Staff Anyone who hears about the tragic death of a 13-year-old California girl after a routine tonsil-removal surgery has to feel for the grieving parents who don’t want her removed from life support. The McMaths refuse to believe that their daughter Jahi, who was declared brain dead more than a week ago, is truly dead because machines are keeping her other organs alive. “How could you not let me have my kid for Christmas?” said Nailah Winkfield, McMath’s mother, in an interview with local reporters. “And this is Children’s Hospital, supposed to be so compassionate, so loving, and I asked, can my daughter just live a few more days? Because she is living.” McMath was declared brain dead more than a week ago, and her family has been fighting with hospital staff at Children’s Hospital & Research Center in Oakland to keep her body in a viable state and have her provided with nutrition via a feeding tube. “To me, it just looks like she’s at peace and she’s resting,” said Jahi’s uncle Omari Sealey, “and when she’s done going through the traumatic stuff that her body’s going through right now, and she feels well enough, she’ll wake up.” But McMath is dead—as horrible as that is for her family to fathom—and leaving her body attached to machines is akin to allowing a corpse remain in a hospital bed without a proper burial. Perhaps hospitals should stop calling such care “life support” since it’s not actually supporting any living person, just a body. “This case is so sad it is almost beyond description,” wrote Arthur Caplan, head of the division of medical ethics at NYU Langone Medical Center in a blog he posted Thursday on the NBC News website. “But that fact should not be a reason to take the view that we don’t know what to do when someone is pronounced brain dead. Brain dead is dead.” © 2013 Boston Globe Media Partners, LLC
Link ID: 19057 - Posted: 12.21.2013
By Ben Thomas 2013’s Nobel prize in Physiology or Medicine honors three researchers in particular – but what it really honors is thirty-plus years of work not only from them, but also from their labs, their graduate students and their collaborators. Winners James Rothman, Randy Schekman and Thomas Südhof all helped assemble our current picture of the cellular machinery that enables neurotransmitter chemicals to travel from one nerve cell to the next. And as all three of these researchers agree, that process of understanding didn’t catalyze until the right lines of research, powered by the right tools, happened to converge at the right time. Long before that convergence, though, these three scientists began by seeking the answers to three different questions – none of which seemed to have anything to do with the others. When James Rothman started out as a researcher at Harvard in 1978, his goal was to find out exactly how vesicle transmission worked. Vesicles – Latin for “little vessels” – are the microscopic capsules that carry neurotransmitter molecules like serotonin and dopamine from one brain cell to another. By the late 1960s, the old-guard biochemist George Palade, along with other researchers, had already deduced that synaptic vesicles are necessary for neurotransmission – but the questions of which proteins guided these tiny vessels on their journey, and how they docked with receiving neurons, remained mysterious. Yale University's James Rothman set out to break down the process of vesicle transmission, chemical-by-chemical, reaction-by-reaction. Courtesy of Yale University. In other words, although researchers had established the existence of this vesicle transmission process, no one knew exactly what made it work, or how. © 2013 Scientific American
Link ID: 19022 - Posted: 12.11.2013
by Bethany Brookshire When neurons throughout the brain and body send messages, they release chemical signals. These chemicals, neurotransmitters, pass into the spaces between neurons, or synapses, binding to receptors to send a signal along. When they are not in use, neurotransmitters are stored within the cell in tiny bubbles called vesicles. During signaling, these vesicles head to the membrane of the neuron, where they dump neurotransmitter into the synapse. And after delivering their cargo, most vesicles disappear. But more vesicles keep forming, filling with neurotransmitters so neurons can keep sending signals. What goes up must come down. When vesicles go out, they must come back. But how fast to the vesicles re-appear? Must faster, it turns out, than we first thought. Neurotransmission happens fast. An electrical signal comes down a neuron in your brain and triggers vesicles to move to the cell membrane. When the vesicles merge into the membrane and release their chemical cargo, the neurotransmitters float across the open synapse to the next neuron. This happens every time the neuron “fires.” This needs to happen very quickly, as neurons often fire at 100 hertz, or 100 times per second. Some neurons perform a “kiss-and-run,” opening up a temporary pore in the membrane, releasing a little bit of neurotransmitter and darting away again. Other vesicles need to merge with the synapse entirely. With the assistance of docking proteins, these vesicles fuse with the membrane of the neuron to release the neurotransmitters, a process called exocytosis. © Society for Science & the Public 2000 - 2013.
Link ID: 19021 - Posted: 12.11.2013
By Helen Briggs BBC News An anti-tuberculosis vaccine could prevent multiple sclerosis, early research suggests. A small-scale study by researchers at the Sapienza University of Rome has raised hopes that the disease can be warded off when early symptoms appear. More research is needed before the BCG vaccine can be trialled on MS patients. The MS Society said the chance to take a safe and effective preventative treatment after a first MS-like attack would be a huge step forward. MS is a disease affecting nerves in the brain and spinal cord, causing problems with muscle movement, balance and vision. Early signs include numbness, vision difficulties or problems with balance. About half of people with a first episode of symptoms go on to develop MS within two years, while 10% have no more problems. In the study, published in the journal Neurology, Italian researchers gave 33 people who had early signs of MS an injection of BCG vaccine. The other 40 individuals in the study were given a placebo. After five years, 30% of those who received the placebo had not developed MS, compared with 58% of those vaccinated. "These results are promising, but much more research needs to be done to learn more about the safety and long-term effects of this live vaccine," said study leader Dr Giovanni Ristori. "Doctors should not start using this vaccine to treat MS or clinically isolated syndrome." BBC © 2013
Keyword: Multiple Sclerosis
Link ID: 19003 - Posted: 12.05.2013
Peter Hildebrand Neuroscience is a rapidly growing field, but one that is usually thought to be too complex and expensive for average Americans to participate in directly. Now, an explosion of cheap scientific devices and online tutorials are on the verge of changing that. This change could have exciting implications for our future understanding of the brain. From 1995 to 2005, the amount of money spent on neuroscience research doubled. A lot of that research used medical devices, like MRI and CT Scan machines, and drugs that everyday citizens don’t have access to. Even in colleges, experience with powerful research equipment is reserved for upperclassmen and graduate students. The lowlier castes can work with models or dissect animal brains, but as scientist and engineer Greg Gage points out in this TED video, the brain isn’t like the heart or the lungs. You can’t tell how it works just by looking at it. Gage is calling for “neuro-revolution,” in which scientists and inventors come together to put the tools for learning neuroscience into the hands of the public. He may be onto something too, because those tools are looking more accessible than ever before. One of the most well publicized examples of this punk rock revolution has been Gage’s own “SpikerBox,” which he co-developed with Tim Marzullo. Roughly the size of your fist, the SpikerBox is a small collection of electronic components bolted between two squares of orange plastic. Coming out of one end are two pins that you can use to record the electrical activity of nerve cells in, say, a recently severed cockroach leg. There’s also a port that allows you to attach the box to a smartphone or tablet, and watch the spikes of activity as the neurons are stimulated. © 2013 Salon Media Group, Inc.
Keyword: Brain imaging
Link ID: 18976 - Posted: 11.26.2013