Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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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
Jessica Wright A tiny fiber-optic probe inserted into the reward center of the mouse brain monitors how the mouse feels about meeting a peer — or a golf ball. The unpublished technique was presented last week at the at the 2013 Society for Neuroscience annual meeting in San Diego. Mice feel the most satisfaction when sniffing another mouse’s rear and when walking away from a golf ball, the study found. The new technique is one of only a few ways to read the electrical activity of neurons in freely moving mice and is the most noninvasive, making it ideal for monitoring social interactions. The method takes advantage of a fluorescent molecule that lights up only in the presence of calcium, which rushes into the cell when neurons fire. The researchers used mice engineered to express this molecule only in neurons that make dopamine — the chemical messenger that mediates a sense of reward — in the ventral tegmental area (VTA). The researchers placed the cable in the VTA, the source of most of the brain’s dopamine neurons. The fiber-optic cable is 400 micrometers in diameter, and could probably be half that size, says Lisa Gunaydin, who developed the method as a graduate student in Karl Deisseroth’s lab at Stanford University in California. When neurons expressing the fluorescent molecule fire, the cable reads these as a series of spikes. In the study, the researchers gave thirsty mice sweet water and, as expected, their dopamine activity in the VTA spiked each time they drank. When the mice interact with a new mouse, or a golf ball, the dopamine neurons fire more on the first encounter but dull with repeated visits, suggesting that the mice are most excited by novelty. © Copyright 2013 Simons Foundation
Keyword: Drug Abuse
Link ID: 18949 - Posted: 11.21.2013
Helen Shen Long used to treat movement disorders, deep-brain stimulation (DBS) is rapidly emerging as an experimental therapy for neuropsychiatric conditions including depression, Tourette’s syndrome, obsessive–compulsive disorder and even Alzheimer’s disease. But despite some encouraging results in patients, it remains largely unknown how the electrical pulses delivered by implants deep within the brain affect neural circuits and change behaviour. Now there is a prototype DBS device that could provide some answers, researchers reported on 10 November at the Society for Neuroscience’s annual meeting in San Diego, California. Called Harmoni, the device is the first DBS implant to monitor electrical and chemical responses in the brain while delivering electrical stimulation. “That’s new data that we haven’t really had access to in humans before,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio, who is not involved in the work. Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project. The results come at a time of great excitement in the DBS field. Last month, the US government's Defense Advanced Research Projects Agency (DARPA) announced a 5-year, US$70-million initiative to support development of the next generation of therapeutic brain-stimulating technologies. © 2013 Nature Publishing Group,
Link ID: 18922 - Posted: 11.13.2013
M. Mitchell Waldrop Kwabena Boahen got his first computer in 1982, when he was a teenager living in Accra. “It was a really cool device,” he recalls. He just had to connect up a cassette player for storage and a television set for a monitor, and he could start writing programs. But Boahen wasn't so impressed when he found out how the guts of his computer worked. “I learned how the central processing unit is constantly shuffling data back and forth. And I thought to myself, 'Man! It really has to work like crazy!'” He instinctively felt that computers needed a little more 'Africa' in their design, “something more distributed, more fluid and less rigid”. Today, as a bioengineer at Stanford University in California, Boahen is among a small band of researchers trying to create this kind of computing by reverse-engineering the brain. The brain is remarkably energy efficient and can carry out computations that challenge the world's largest supercomputers, even though it relies on decidedly imperfect components: neurons that are a slow, variable, organic mess. Comprehending language, conducting abstract reasoning, controlling movement — the brain does all this and more in a package that is smaller than a shoebox, consumes less power than a household light bulb, and contains nothing remotely like a central processor. To achieve similar feats in silicon, researchers are building systems of non-digital chips that function as much as possible like networks of real neurons. Just a few years ago, Boahen completed a device called Neurogrid that emulates a million neurons — about as many as there are in a honeybee's brain. And now, after a quarter-century of development, applications for 'neuromorphic technology' are finally in sight. © 2013 Nature Publishing Group
By Bradley E. Alger, Ph.D. Cannabis, derived from a plant and one of the oldest known drugs, has remained a source of controversy throughout its history. From debates on its medicinal value and legalization to concerns about dependency and schizophrenia, cannabis (marijuana, pot, hashish, bhang, etc.) is a hot button for politicians and pundits alike. Fundamental to understanding these discussions is how cannabis affects the mind and body, as well as the body’s cells and systems. How can something that stimulates appetite also be great for relieving pain, nausea, seizures, and anxiety? Whether its leaves and buds are smoked, baked into pastries, processed into pills, or steeped as tea and sipped, cannabis affects us in ways that are sometimes hard to define. Not only are its many facets an intrinsically fascinating topic, but because they touch on so many parts of the brain and the body, their medical, ethical, and legal ramifications are vast. The intercellular signaling molecules, their receptors, and synthetic and degradative enzymes from which cannabis gets its powers had been in place for millions of years by the time humans began burning the plants and inhaling the smoke. Despite records going back 4,700 years that document medicinal uses of cannabis, no one knew how it worked until 1964. That was when Yechiel Gaoni and Raphael Mechoulam1 reported that the main active component of cannabis is tetrahydrocannabinol (THC). THC, referred to as a “cannabinoid” (like the dozens of other unique constituents of cannabis), acts on the brain by muscling in on the intrinsic neuronal signaling system, mimicking a key natural player, and basically hijacking it for reasons best known to the plants. Since the time when exogenous cannabinoids revealed their existence, the entire natural complex came to be called the “endogenous cannabinoid system,” or “endocannabinoid system” (ECS). Copyright 2013 The Dana Foundation
Keyword: Drug Abuse
Link ID: 18874 - Posted: 11.06.2013
by Anil Ananthaswamy THE first clinical trial aimed at boosting social skills in people with autism using magnetic brain stimulation has been completed – and the results are encouraging. "As a first clinical trial, this is an excellent start," says Lindsay Oberman of the Beth Israel Deaconess Medical Centre in Boston, who was not part of the study. People diagnosed with autism spectrum disorder often find social interactions difficult. Previous studies have shown that a region of the brain called the dorsomedial prefrontal cortex (dmPFC) is underactive in people with autism. "It's also the part of the brain linked with understanding others' thoughts, beliefs and intentions," says Peter Enticott of Monash University in Melbourne, Australia. Enticott and his colleagues wondered whether boosting the activity of the dmPFC using repetitive transcranial magnetic stimulation (rTMS), which involves delivering brief but strong magnetic pulses through the scalp, could help individuals with autism deal with social situations. So the team carried out a randomised, double-blind clinical trial – the first of its kind – involving 28 adults diagnosed with either high-functioning autism or Asperger's syndrome. Some participants received 15 minutes of rTMS for 10 days, while others had none, but experienced all other aspects, such as having coils placed on their heads and being subjected to the same sounds and vibrations. © Copyright Reed Business Information Ltd.
Link ID: 18863 - Posted: 11.02.2013
/ by Charles Choi, LiveScience Using lasers, scientists can now surgically blast holes thinner than a human hair in the heads of live fruit flies, allowing researchers to see how the flies' brains work. Microscopically peering into living animals can help scientists learn more about key details of these animals' biology. For instance, tiny glass windows surgically implanted into the sides of living mice can help researchers study how cancers develop in real time and evaluate the effectiveness of potential medicines. Surgically preparing small live animals for such "intravital microscopy" is often time-consuming and requires considerable skill and dexterity. Now, Supriyo Sinha, a systems engineer at Stanford University in California, and his colleagues have developed a way to prepare live animals for such microscopy that is both fast -- taking less than a second -- and largely automated. To conduct this procedure, scientists first cooled fruit flies to anesthetize them. Then, the researchers carefully picked up the insects with tweezers and glued them to the tops of glass fibers in order to immobilize the flies' bodies and heads. Then, using a high-energy pulsed ultraviolet laser, the researchers blasted holes measuring 12 to 350 microns wide in the flies' heads. (In comparison, the average human hair is about 100 microns wide.) They then applied a saline solution to exposed tissue to help keep the fly brains healthy. © 2013 Discovery Communications, LLC.
Link ID: 18861 - Posted: 11.02.2013
By KATE MURPHY Whether it’s hitting a golf ball, playing the piano or speaking a foreign language, becoming really good at something requires practice. Repetition creates neural pathways in the brain, so the behavior eventually becomes more automatic and outside distractions have less impact. It’s called being in the zone. But what if you could establish the neural pathways that lead to virtuosity more quickly? That is the promise of transcranial direct current stimulation, or tDCS — the passage of very low-level electrical current through targeted areas of the brain. Several studies conducted in medical and military settings indicate tDCS may bring improvements in cognitive function, motor skills and mood. Some experts suggest that tDCS might be useful in the rehabilitation of patients suffering from neurological and psychological disorders, perhaps even in reducing the time and expense of training healthy people to master a skill. But the research is preliminary, and now there is concern about a growing do-it-yourself community, many of them video gamers, who are making tDCS devices with nine-volt batteries to essentially jump-start their brains. “If tDCS is powerful enough to do good, you have to wonder if, done incorrectly, it could cause harm,” said Dr. H. Branch Coslett, chief of the cognitive neurology section at the University of Pennsylvania School of Medicine and a co-author of studies showing that tDCS improves recall of proper names, fosters creativity and improves reading efficiency. Even the tDCS units used in research are often little more than a nine-volt battery with two electrodes and a controller for setting the current and the duration of the session. Several YouTube videos show how to make a rough facsimile. © 2013 The New York Times Company
Link ID: 18848 - Posted: 10.29.2013
by Tina Hesman Saey BOSTON — A variant in a gene involved in breaking down chemicals in smoke triples a smoker’s risk of multiple sclerosis, a study shows. Smoking increases by 30 to 50 percent a person’s risk of multiple sclerosis, a disease in which the immune system attacks a waxy coating around nerve cells. Scientists don’t know exactly how smoking contributes to the disease. Farren Briggs of the University of California, Berkeley and his colleagues searched DNA of thousands of people in Northern California, Norway and Sweden for genetic variants associated with both smoking and multiple sclerosis. The team found hundreds of variants in three genes involved in breaking down chemicals found in smoke, Briggs said October 24 at the annual meeting of the American Society of Human Genetics. In particular, people who smoke and who have two copies of a variant in the NAT1 gene have a risk of getting MS that is three times higher than that of smokers without the variant. For nonsmokers, the variant doesn’t increase MS risk. Citations F.B.S. Briggs et al. NAT1 in an important genetic effect modifier of tobacco smoke exposure in multiple sclerosis susceptibility in 5,453 individuals. American Society of Human Genetics annual meeting, Boston, October 24, 2013. Further Reading N. Seppa. Old drug may have new trick. Science News. Vol. 184, November 2, 2013, p. 16. N. Seppa. Black women may have highest multiple sclerosis rates. Science News. Vol. 183, June 15, 2013, p. 15. © Society for Science & the Public 2000 - 2013