Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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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
Special Note to Teachers: The content of the following lesson plans compares the “normal” brain to a “zombie” brain. Zombies are not real but there are plenty of diseases that effect real people and students may have people in their lives who have suffered because of them. The following lessons about neuroscience have been inspired by the book, “The Zombie Autopsies”, written by Steven C. Schlozman, M.D., and are intended to compliment it. “The Zombie Autopsies” was inspired by George Romero’s 1968 cult-classic horror film “Night of the Living Dead”. These original lessons build upon each other and have an accompanying plot line where the world is fighting a zombie apocalypse and the best and the brightest young people are being trained as medical students – with a specialty in neuroscience – with the hopes that they will be able to provide a cure to this terrible epidemic and save humanity. For a richer experience have the students read the book in class and as homework (see suggested reading schedule) along with the class activities. Although the materials are organized as a unit, lessons can be used as stand-alone or can be shaped to fit the needs of you and your students regarding time and content. For example, Lesson 3 is perfect for the day of Halloween. © 2013 MacNeil-Lehrer Productions
Keyword: Learning & Memory
Link ID: 18824 - Posted: 10.23.2013
A narrowing of the veins from the brain is unlikely as a cause multiple sclerosis, say researchers from B.C. and Saskatchewan who found the narrowing is a common and normal finding in most people. Italian Paolo Zamboni made headlines in Canada four years ago for his belief that clearing blocked or narrowed neck veins could relieve MS symptoms. Since then probably more than 3,000 Canadians have gone out of country for dilation treatment, said Dr. Anthony Traboulsee of the University of British Columbia. In Tuesday's online issue of the The Lancet, Traboulsee and his co-authors published their findings on the prevalence of narrowing, known as chronic cerebrospinal venous insufficiency or CCSVI, in people with MS, their siblings and unrelated healthy controls. Using catheter venography to directly visualize veins, the researchers found three people tested positive for CCSVI: One of 65 (2 per cent) of those with MS. One of 46 (2 per cent) of siblings. One of 32 (3 per cent) on unrelated controls. "This was a big surprise to all of us," Traboulsee told reporters. "We were really expecting to find many more people with this feature." When the researchers used ultrasound to look for CCSVI, they found narrowing in more than 50 per cent of all three groups. The hypothesis that vein narrowing has a role in the cause of MS is unlikely since its prevalence was similar in all three groups, the study's authors concluded. © CBC 2013
Keyword: Multiple Sclerosis
Link ID: 18765 - Posted: 10.09.2013
At the TEDx conference in Detroit last week, RoboRoach #12 scuttled across the exhibition floor, pursued not by an exterminator but by a gaggle of fascinated onlookers. Wearing a tiny backpack of microelectronics on its shell, the cockroach—a member of the Blaptica dubia species—zigzagged along the corridor in a twitchy fashion, its direction controlled by the brush of a finger against an iPhone touch screen (as seen in video above). RoboRoach #12 and its brethren are billed as a do-it-yourself neuroscience experiment that allows students to create their own “cyborg” insects. The roach was the main feature of the TEDx talk by Greg Gage and Tim Marzullo, co-founders of an educational company called Backyard Brains. After a summer Kickstarter campaign raised enough money to let them hone their insect creation, the pair used the Detroit presentation to show it off and announce that starting in November, the company will, for $99, begin shipping live cockroaches across the nation, accompanied by a microelectronic hardware and surgical kits geared toward students as young as 10 years old. That news, however, hasn’t been greeted warmly by everyone. Gage and Marzullo, both trained as neuroscientists and engineers, say that the purpose of the project is to spur a “neuro-revolution” by inspiring more kids to join the fields when they grow up, but some critics say the project is sending the wrong message. "They encourage amateurs to operate invasively on living organisms" and "encourage thinking of complex living organisms as mere machines or tools," says Michael Allen Fox, a professor of philosophy at Queen's University in Kingston, Canada. © 2013 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 18755 - Posted: 10.08.2013
By Julianne Chiaet It has taken a century so far for scientists to not figure out the cause of multiple sclerosis (MS). The inflammatory disease, which affects more than 2.1 million people worldwide, has been blamed on toxins, viruses and even food. Most recently, scientists have placed their bets on two major ideas: The first (and far more popular) hypothesis suggests MS begins in white matter, which influences how parts of the brain work together. White matter consists of bundles of axons covered in myelin, a white insulating fatty layer. In people with MS myelin degrades and nerve fibers are left exposed, causing problems in motor coordination and loss of senses. The second hypothesis suggests that MS begins in the gray matter, which affects thinking and learning. The white matter hypothesis overshadows its alternative in part because white matter’s impact is easier to observe. When using a microscope to look at brain tissue, scientists are struck by the degradation in the myelin in samples from patients with MS. And when analyzing MS in the clinic, the overt symptoms experienced by a person with the disease can be attributed to the myelin. Symptoms associated with dysfunctions in gray matter are less obvious, such as the loss of an IQ point. Now, new evidence lends support to the less-favored gray matter hypothesis. Scientists at Rutgers University in Newark tried a new approach to look into the gray matter of MS patients. They analyzed proteins in cerebrospinal fluid (CSF), which can be thought of as the central nervous system’s “blood.” By comparing the quantity of specific CSF proteins in patients who were newly diagnosed or had the relapsing remitting variety of MS with that of healthy patients, the researchers found an uneven distribution of 20 proteins among the three groups. © 2013 Scientific American
by Andy Coghlan Parts of the brain may still be alive after a person's brain activity is said to have flatlined. When someone is in a deep coma, their brain activity can go silent. An electroencephalogram measuring this activity may eventually show a flatline, usually taken as a sign of brain death. However, while monitoring a patient who had been placed in a deep coma to prevent seizures following a cardiac arrest, Bogdan Florea, a physician at the Regina Maria Medical Centre in Cluj-Napoca, Romania, noticed a strange thing – some tiny intermittent bursts of activity were interrupting an otherwise flatline signal, each lasting a few seconds. He asked Florin Amzica of the University of Montreal in Canada and his colleagues to investigate what might be happening. To imitate what happened in the patient, Amzica's team put cats into a deep coma using a high dose of anaesthesia. While EEG recordings taken from the surface of the brain – the cortex – showed a flatline, recordings from deep-brain electrodes revealed tiny bursts of activity originating in the hippocampus, responsible for memory and learning, which spread within minutes to the cortex. "These ripples build up a synchrony that rises in a crescendo to reach a threshold where they can spread beyond the hippocampus and trigger activity in the cortex," says Amzica. © Copyright Reed Business Information Ltd.
Link ID: 18683 - Posted: 09.21.2013