Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

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Kerri Smith Marta Zlatic owns what could be the most tedious film collection ever. In her laboratory at the Janelia Research Campus in Ashburn, Virginia, the neuroscientist has stored more than 20,000 hours of black-and-white video featuring fruit-fly (Drosophila) larvae. The stars of these films are doing mundane maggoty things, such as wriggling and crawling about, but the footage is helping to answer one of the biggest questions in modern neuroscience: how the circuitry of the brain creates behaviour. It's a major goal across the field: to work out how neurons wire up, how signals move through the networks and how these signals work together to pilot an animal around, to make decisions or — in humans — to express emotions and create consciousness. Even under the most humdrum conditions — “normal lighting; no sensory cues; they're not hungry”, says Zlatic — her fly larvae can be made to perform 30 different actions, including retracting or turning their heads, or rolling. The actions are generated by a brain comprising just 15,000 neurons. That is nothing compared with the 86 billion in a human brain, which is one of the reasons Zlatic and her teammates like the maggots so much. “At the moment, really, the Drosophila larva is the sweet spot,” says Albert Cardona, Zlatic's collaborator and husband, who is also at Janelia. “If you can get the wiring diagram, you have an excellent starting point for seeing how the central nervous system works.” © 2017 Macmillan Publishers Limited

Keyword: Brain imaging
Link ID: 23944 - Posted: 08.10.2017

Michael Viney I first saw them by night, or rather by flashlight aimed beside the dinghy as we fished a mile beyond Brighton’s pier. A whole shoal of them appeared beneath the boat, waving their arms, their button eyes glistening. We were not fishing for squid – too foreign a taste for England in those days. But this early glimpse left me fascinated with their kind, not least their giant, still greatly mysterious relative with eyes the size of hubcaps. The Brighton squids were the regular, long-fin Doryteuthis of inshore waters, not the huge, deep-water Architeuthis dux, snared this summer as trawler by-catch on the Porcupine Bank. The Cú na Mara (a nice echo) landed two separate specimens at Dingle a few weeks apart. Expiring on they way up, each was around 6m long, counting in the tentacles. They brought to seven the number landed in 350 years, including a remarkable three in 1995 alone. Two of those were trawled from the Porcupine Bank by a Marine Institute survey vessel. Dr Kevin Flannery, the Dingle marine biologist, would now like the institute to send its remote cameras for a proper look around. Meanwhile, the second squid, as dead as the first but in better shape, will soon be on display in the Dingle Oceanworld aquarium. What could seem strangest is that giant squid are soft-bodied molluscs, like limpets or winkles. Abandoning external shells to work on jet propulsion, they have developed genes and nerves of special interest to science. © 2017 THE IRISH TIMES

Keyword: Miscellaneous
Link ID: 23923 - Posted: 08.07.2017

Brandie Jefferson It wasn't long ago that there were no treatments for multiple sclerosis. In the 1970s, some doctors used chemotherapy to treat the degenerative neurological disease. Since then, more than a dozen drugs have been developed or approved, including infusions, oral medications and self-administered shots. None of these are a magic bullet for a disease that can be disabling and deadly. But now there is a new drug, Ocrevus, that looks like a game-changer. It uses a novel approach to blocking the inflammation that drives the disease and looks as if it's spectacularly effective. It also costs $65,000 a year. I have MS. Should I take Ocrevus? That, I discovered, is not a simple question to answer. But because I'm an MS patient and a science journalist, I was determined to try to figure it out. In March, the FDA approved Ocrevus (ocrelizumab) for the treatment of relapsing-remitting multiple sclerosis, the most common form of the disease. People with RRMS tend to have flare-ups when their symptoms worsen, followed by periods of remission and, in some cases, a full or partial recovery. In two clinical trials sponsored by the drug's eventual manufacturer, F. Hoffmann-La Roche, RRMS patients who were given ocrelizumab had about 50 percent fewer relapses and up to 95 percent fewer new lesions on the brain and spinal cord than those who were given Rebif, a common therapy. MS is an autoimmune disease, meaning the body attacks itself. The body's nerve endings and the fatty tissue that coats them, called myelin, bear the brunt of the immune system's attacks. As a result, the central nervous system has difficulty communicating with the nerves, leading to a disease that manifests itself in different ways, such as pain, fatigue, disability and slurred speech. © 2017 npr

Keyword: Multiple Sclerosis
Link ID: 23838 - Posted: 07.14.2017

By Matthew Hutson Artificial neural networks, computer algorithms that take inspiration from the human brain, have demonstrated fancy feats such as detecting lies, recognizing faces, and predicting heart attacks. But most computers can’t run them efficiently. Now, a team of engineers has designed a computer chip that uses beams of light to mimic neurons. Such “optical neural networks” could make any application of so-called deep learning—from virtual assistants to language translators—many times faster and more efficient. “It works brilliantly,” says Daniel Brunner, a physicist at the FEMTO-ST Institute in Besançon, France, who was not involved in the work. “But I think the really interesting things are yet to come.” Most computers work by using a series of transistors, gates that allow electricity to pass or not pass. But decades ago, physicists realized that light might make certain processes more efficient—for example, building neural networks. That’s because light waves can travel and interact in parallel, allowing them to perform lots of functions simultaneously. Scientists have used optical equipment to build simple neural nets, but these setups required tabletops full of sensitive mirrors and lenses. For years, photonic processing was dismissed as impractical. Now, researchers at the Massachusetts Institute of Technology (MIT) in Cambridge have managed to condense much of that equipment to a microchip just a few millimeters across. © 2017 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 23758 - Posted: 06.21.2017

By Neuroskeptic A high-profile paper in Cell reports on a new brain stimulation method that’s got many neuroscientists excited. The new technique, called temporal interference (TI) stimulation, is said to be able to reach structures deep inside the brain, using nothing more than scalp electrodes. Currently, the only way to stimulate deep brain structures is by implanting electrodes (wires) into the brain – which is an expensive and potentially dangerous surgical procedure. TI promises to make deep brain stimulation an everyday, non-invasive tool. But will it really work? The paper comes from Nir Grossman et al. from the lab of Edward S. Boyden at MIT. Their technique is based around applying two electrical fields to the subject’s head. Each field is applied using two scalp electrodes. It is the interaction between the two fields that creates brain stimulation. Both fields oscillate at slightly different frequencies, for instance 2 kHz and 2.01 kHz. Where these fields overlap, a pattern of interference is created which oscillates with an ‘envelope’ at a much lower frequency, say 10 Hz. The frequency of the two fields is too high to have any effect on neural activity, but the interference pattern does have an effect. Crucially, while the electric fields are strongest close to the electrodes, the interference pattern is most intense at a remote point – which could be deep in the brain.

Keyword: Brain imaging; Parkinsons
Link ID: 23740 - Posted: 06.14.2017

In a pair of studies, scientists at the National Institutes of Health explored how the human brain stores and retrieves memories. One study suggests that the brain etches each memory into unique firing patterns of individual neurons. Meanwhile, the second study suggests that the brain replays memories faster than they are stored. The studies were led by Kareem Zaghloul, M.D., Ph.D., a neurosurgeon-researcher at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Persons with drug resistant epilepsy in protocols studying surgical resection of their seizure focus at the NIH’s Clinical Center enrolled in this study. To help locate the source of the seizures, Dr. Zaghloul’s team surgically implanted a grid of electrodes into the patients’ brains and monitored electrical activity for several days. “The primary goal of these recordings is to understand how to stop the seizures. However, it’s also a powerful opportunity to learn how the brain works,” said Dr. Zaghloul. For both studies, the researchers monitored brain electrical activity while testing the patients’ memories. The patients were shown hundreds of pairs of words, like “pencil and bishop” or “orange and navy,” and later were shown one of the words and asked to remember its pair. In one study, published in the Journal of Neuroscience, the patients correctly remembered 38 percent of the word pairs they were shown. Electrical recordings showed that the brain waves the patients experienced when they correctly stored and remembered a word pair often occurred in the temporal lobe and prefrontal cortex regions. Nevertheless, the researchers showed that the waves that appeared when recalling the words happened faster than the waves that were present when they initially stored them as memories.

Keyword: Learning & Memory; Epilepsy
Link ID: 23704 - Posted: 06.03.2017

Mo Costandi Since 1997, more than 100,000 Parkinson’s Disease patients have been treated with deep brain stimulation (DBS), a surgical technique that involves the implantation of ultra-thin wire electrodes. The implanted device, sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a structure called the subthalamic nucleus, located near the centre of the brain, and effectively alleviates many of the physical symptoms of the disease, such as tremor, muscle rigidity, and slowed movements. DBS is generally safe but, like any surgical procedure, comes with some risks. First and foremost, it is highly invasive, requiring small holes to be drilled in the patient’s skull, through which the electrodes are inserted. Potential complications of this include infection, stroke, and bleeding on the brain. The electrodes, which are implanted for long periods of time, sometimes move out of place; they can also cause swelling at the implantation site; and the wire connecting them to the battery, typically placed under the skin of the chest, can erode, all of which require additional surgical procedures. Now, researchers at the Massachusetts Institute of Technology have a developed a new method that can stimulate cells deep inside the brain non-invasively, using multiple electric fields applied from outside the organ. In a study published today in the journal Neuron, they show that the method can selectively stimulate deep brain structures in live mice, without affecting the activity of cells in the overlying regions, and also that it can be easily adjusted to evoke movements by stimulation of the motor cortex. © 2017 Guardian News and Media Limited o

Keyword: Parkinsons
Link ID: 23700 - Posted: 06.02.2017

By Gary Stix In April, DARPA announced contracts for a program to develop practical methods to help someone learn more quickly. In the ensuing press coverage, the endeavor drew immediate comparisons to the The Matrix—in which Neo, the Keanu Reeves character, has his brain reprogrammed so that he instantly masters Kung Fu. DARPA is known for setting ambitious goals for its technology development programs. But it is not requiring contractors for the $50 million, four-year effort to find a way to let a special forces soldier upload neural codes to instantaneously execute a flawless Wushu butterfly kick. The agency did award contracts, though, to find some means of zapping nerves in the peripheral nervous system outside the brain to speed the rate at which a foreign language can be learned by as much as 30 percent, a still not-too-shabby goal. Sending an electrical current into the vagus nerve in the neck from a surgically implanted device is already approved for treating epilepsy and depression. The DARPA program, in tacit acknowledgement that mandatory surgery might be unacceptable for students contemplating an accelerated Mandarin class, wants to develop a non-invasive device to stimulate a peripheral nerve, perhaps in the ear. The goal is to hasten, not just the learning of foreign languages, but also to facilitate pattern recognition tasks such as combing through surveillance imagery. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 23699 - Posted: 06.02.2017

A cannabis compound has been proven for the first time to reduce the frequency of seizures in people with a rare, severe form of epilepsy, according to the results of a randomized trial. For years, parents have pointed to anecdotal benefits of cannabidiol (CBD), a compound in the marijuana plant that does not produce a high, saying it reduces seizures in treatment-resistant epilepsy. Now doctors have performed a randomized trial to show cause and effect, with the findings published in Wednesday's issue of the New England Journal of Medicine. To conduct the study, the researchers focused on Dravet syndrome, a rare form of epilepsy that begins in infancy and is linked to a particular mutation that often resists combinations of up to 10 conventional seizure medications. They enrolled 120 patients who ranged in age from 2.5 to 18 years. Sixty-one patients were randomly assigned to cannabidiol, and the 59 others to placebo. Neither the researchers nor the families knew who received the medication to prevent bias. All continued to take their existing medications. "The message is that cannabidiol does work in reducing convulsing seizures in children with Dravet syndrome," said lead author Dr. Orrin Devinksy, who is director of NYU's Langone Comprehensive Epilepsy Center. For those in the cannabinoid group, the median number of convulsive seizures per month dropped from 12.4 per month before treatment, to 5.9 seizures, the researchers reported. The placebo group, in comparison, only saw their convulsive seizures fall from 14.9 per month, to 14.1. ©2017 CBC/Radio-Canada.

Keyword: Epilepsy; Drug Abuse
Link ID: 23659 - Posted: 05.25.2017

By Esther Landhuis On the heels of one failed drug trial after another, a recent study suggests people with early Alzheimer’s disease could reap modest benefits from a device that uses magnetic fields to produce small electric currents in the brain. Alzheimer’s is a degenerative brain disorder that afflicts more than 46 million people worldwide. At present there are no treatments that stop or slow its progression, although several approved drugs offer temporary relief from memory loss and other cognitive symptoms by preventing the breakdown of chemical messengers among nerve cells. The new study tested a regimen that combines computerized cognitive training with a procedure known as repetitive transcranial magnetic stimulation (rTMS). The U.S. Food and Drug Administration has cleared rTMS devices for some migraine sufferers as well as for people with depression who have not responded to antidepressant medications. Last month at the 13th International Conference on Alzheimer’s and Parkinson’s Diseases in Vienna, Israel-based Neuronix reported results of a phase III clinical trial of its therapy system, known as neuroAD, in Alzheimer’s patients. More than 99 percent of Alzheimer’s drug trials have failed. The last time a phase III trial for a wholly new treatment succeeded (not just a combination of two already approved drugs) was about 15 years ago. The recent study did not test a drug but rather a device, which usually has an easier time gaining FDA clearance. NeuroAD has been approved for use in Europe and the U.K., where six weeks of therapy costs about $6,700. The system is not commercially available in the U.S., but based on the latest results the company submitted an application for FDA clearance last fall. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23635 - Posted: 05.19.2017

Jon Hamilton Tiny, 3-D clusters of human brain cells grown in a petri dish are providing hints about the origins of disorders like autism and epilepsy. An experiment using these cell clusters — which are only about the size of the head of a pin — found that a genetic mutation associated with both autism and epilepsy kept developing cells from migrating normally from one cluster of brain cells to another, researchers report in the journal Nature. "They were sort of left behind," says Dr. Sergiu Pasca, an assistant professor of psychiatry and behavioral sciences at Stanford. And that type of delay could be enough to disrupt the precise timing required for an actual brain to develop normally, he says. The clusters — often called minibrains, organoids or spheroids — are created by transforming skin cells from a person into neural stem cells. These stem cells can then grow into structures like those found in the brain and even form networks of communicating cells. Brain organoids cannot grow beyond a few millimeters in size or perform the functions of a complete brain. But they give scientists a way to study how parts of the brain develop during pregnancy. "One can really understand both a process of normal human brain development, which we frankly don't understand very well, [and] also what goes wrong in the brain of patients affected by diseases," says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard who was not involved in the cell migration study. Arlotta is an author of a second paper in Nature about creating a wide variety of brain cells in brain organoids. © 2017 npr

Keyword: Development of the Brain; Autism
Link ID: 23545 - Posted: 04.27.2017

By KAREN BARROW The World Health Organization estimates that more than 50 million people worldwide have some form of epilepsy, a neurological disorder that is characterized by recurring episodes of seizure. While seizures come in various forms, those with epilepsy cope with similar issues: social stigma, complex treatment options and a feeling of powerlessness. Here, eight men, women and children discuss what it’s like to live with epilepsy. Denise L. Pease, an assistant comptroller for New York City, began having complex partial seizures after a car accident in which she suffered a traumatic brain injury. But because Ms. Pease lives alone, it wasn’t until a relative saw her having a tonic-clonic seizure, what used to be known as a grand mal seizure, that she realized she had developed epilepsy. Tonic-clonic seizures typically involve the whole body and can be very dramatic. Ms. Pease began to notice that she would get a strange taste in her mouth before a seizure, so whenever that happened she made sure she was seated in a safe location and waited for the seizure to pass. This sensation of an oncoming seizure, called an aura, is common among people with epilepsy. After eight years of trying different medications to control her epilepsy, Ms. Pease is happy to be back at work and no longer lives in fear of an imminent seizure. Ms. Pease is hopeful that she will soon be able to drive, and she continues to plan for her future. “When you have epilepsy, you have to be your own advocate,” she said. Sallie Gallagher’s son, Michael, started having complex partial seizures at age 4. This type of seizure doesn’t cause the full-body twitching associated with tonic-clonic seizure, but it can cause a person to start to act strangely or be completely unaware of his surroundings. © 2017 The New York Times Company

Keyword: Epilepsy
Link ID: 23544 - Posted: 04.27.2017

By BENEDICT CAREY Well-timed pulses from electrodes implanted in the brain can enhance memory in some people, scientists reported on Thursday, in the most rigorous demonstration to date of how a pacemaker-like approach might help reduce symptoms of dementia, head injuries and other conditions. The report is the result of decades of work decoding brain signals, helped along in recent years by large Department of Defense grants intended to develop novel treatments for people with traumatic brain injuries, a signature wound of the Iraq and Afghanistan wars. The research, led by a team at the University of Pennsylvania, is published in the journal Current Biology. Previous attempts to stimulate human memory with implanted electrodes had produced mixed results: Some experiments seemed to sharpen memory, but others muddled it. The new paper resolves this confusion by demonstrating that the timing of the stimulation is crucial. Zapping memory areas when they are functioning poorly improves the brain’s encoding of new information. But doing so when those areas are operating well — as they do for stretches of the day in most everyone, including those with deficits — impairs the process. “We all have good days and bad days, times when we’re foggy, or when we’re sharp,” said Michael Kahana, who with Youssef Ezzyat led the research team. “We found that jostling the system when it’s in a low-functioning state can jump it to a high-functioning one.” Researchers cautioned that implantation is a delicate procedure and that the reported improvements may not apply broadly. The study was of epilepsy patients; scientists still have much work to do to determine whether this approach has the same potential in people with other conditions, and if so how best to apply it. But in establishing the importance of timing, the field seems to have turned a corner, experts said. © 2017 The New York Times Company

Keyword: Learning & Memory; Epilepsy
Link ID: 23520 - Posted: 04.21.2017

By David Noonan Like many people with epilepsy, Richard Shane, 56, has some problems with memory. But he can easily recall his first seizure, 34 years ago. “I was on the phone with my father, and I noticed that I started moaning, and I lost some level of consciousness,” Shane says. After experiencing a similar episode three weeks later, he went to a doctor and learned he had epilepsy, a neurological disorder caused by abnormal electrical activity in the brain. The first medication he was prescribed, Dilantin (phenytoin), failed to stop or even reduce his seizures. So did the second and the third. His epilepsy, it turned out, was drug-resistant. Over the next 22 years Shane suffered two to five or more seizures a week. He and his doctors tried every new antiseizure drug that came along, but none worked. Finally, in 2004, as a last resort, a neurosurgeon removed a small part of Shane's brain where his seizures originated. “It was a matter of what sucks less,” Shane says, “having brain surgery or having epilepsy.” Shane has been seizure-free ever since. As many as three million people in the U.S. live with epilepsy, and more than 30 percent of them receive inadequate relief from medication, a number that persists despite the introduction of more than a dozen new antiepileptic drugs since 1990. Although surgery has helped some patients such as Shane, uncontrollable epilepsy remains a living nightmare for patients and an intractable foe for clinicians and researchers. “I hate to say it, but we do not know why” some people respond to medications and others do not, says neurologist Michael Rogawski, who studies epilepsy treatments at the University of California, Davis. And yet if the central conundrum continues, so does the determined quest for new and different approaches to treating the toughest cases. © 2017 Scientific American

Keyword: Epilepsy
Link ID: 23495 - Posted: 04.15.2017

Consider two children who have childhood absence epilepsy (CAE), the most common form of pediatric epilepsy. They both take the same drug — one child sees an improvement in their seizures, but the other does not. A new study in the Annals of Neurology identified the genes that may underlie this difference in treatment outcomes, suggesting there may be potential for using a precision medicine approach to help predict which drugs will be most effective to help children with CAE. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), both part of the National Institutes of Health. “A better understanding of genetic factors underlying a disease and the way that people respond to treatments may help healthcare providers select the best therapies for children with CAE,” said Vicky Whittemore, Ph.D., program director at NINDS. A team led by Tracy A. Glauser, M.D., director of the Comprehensive Epilepsy Center at Cincinnati Children’s Hospital Medical Center and professor of pediatrics in the University of Cincinnati College of Medicine, investigated whether there may be a genetic basis for different responses to three drugs used for CAE (ethosuximide, valproic acid, and lamotrigine). The experiments focused on three genes that code for T-type calcium channels that are involved in CAE and one gene that codes for a transporter that shuttles the drugs out of the brain. T-type calcium channels help control the firing rate of brain cells. The current study is part of a 32-center, randomized, controlled clinical trial that compared the effects of the three most commonly used drugs in 446 children who were recently diagnosed with CAE.

Keyword: Epilepsy; Genes & Behavior
Link ID: 23480 - Posted: 04.12.2017

By Jia Naqvi An experimental technique reduces the tics, or involuntary movements and vocal outbursts, associated with severe Tourette's syndrome in young adults, a study published Friday found. The surgical technique, called thalamic deep brain stimulation (DBS), sends electrical impulses to a specific area of the brain that reduces the tics, according to the study published in the Journal of Neurosurgery. The finding adds to the growing body of evidence about the safety and effectiveness of deep brain stimulation, which might eventually lead the Food and Drug Administration to approve the treatment for Tourette's syndrome, according to the researchers. “Our study shows that deep brain stimulation is a safe, effective treatment for young adults with severe Tourette syndrome that cannot be managed with current therapies,” said Alon Mogilner, an associate professor in the departments of neurosurgery and anesthesiology at New York University Langone and director of its Center for Neuromodulation, in a news release. “This treatment has the potential to improve the quality of life for patients who are debilitated through their teenage years and young adulthood.” Tourette's syndrome, a type of neurological disorder, according to various studies afflicts from 0.3 to 0.6 percent of children in the United States, with around 138,000 ages 6 to 17 being diagnosed with the condition. The causes for the syndrome are not well known and are thought to be largely genetic, with unidentified environmental factors increasing the likelihood of the condition. Usually the syndrome begins in childhood and the condition improves with age for some people, but for others the symptoms become more severe to the point that people become socially isolated and unable to work or attend school. © 1996-2017 The Washington Post

Keyword: Tourettes
Link ID: 23468 - Posted: 04.08.2017

Sallie Baxendale, Temporal lobe epilepsy—a common form of epilepsy characterized by seizures that begin in the memory-regulating temporal lobe—does appear to influence personality, though not in the way many may think and certainly not in the way people have believed throughout history. The idea of the epileptic personality is an ancient one. Thousands of years ago people with epilepsy were thought to be possessed by either divine beings or demons. In fact, the notion that a seizure represents a kind of communion with another spiritual realm still holds sway in some societies today. In more recent history, Westerners largely perceived epilepsy as a punishment for morally lax behavior. In one 1892 paper, the author claimed that debauchery and excessive lust frequently led to epilepsy and that a person could trigger a seizure by listening to love songs and eating chocolate. More recently, scientists began investigating whether epilepsy, in fact, altered personality. In 1975 neurologists Stephen Waxman and Norman Geschwind, both then at Harvard University, published an analysis based on observations of their patients with temporal lobe epilepsy in which they reported that many patients had a tendency toward religiosity, intense emotions, detailed thoughts, and a compulsion to write or draw. This cluster of characteristics became known as the epileptic personality. Over the next decade other researchers added hostility, aggression, lack of humor and obsessiveness to the list of personality traits supposedly associated with the condition. © 2017 Scientific American

Keyword: Epilepsy; Emotions
Link ID: 23464 - Posted: 04.08.2017

Katherine Whalley The mammalian suprachiasmatic nucleus (SCN) can autonomously generate circadian oscillations in gene expression and neuronal activity, enabling it to fulfil its role as the brain's 'master circadian clock'. Although the contributions of specific neuronal populations to SCN function have begun to be elucidated, the potential influences of SCN astrocytes are relatively unexplored. Brancaccio et al. now reveal an important role for astrocyte–neuron signalling in SCN timekeeping. SCN neurons exhibit circadian oscillations in their intracellular calcium level ([Ca2+]i), peaking during the circadian 'day'. To determine whether similar fluctuations in activity are observed in astrocytes, the authors expressed a genetically encoded reporter of astrocytic [Ca2+]i in organotypic SCN slices. Long-term imaging revealed the presence of circadian oscillations in astrocytic [Ca2+]i, which was at its highest during the circadian 'night' and thus was anti-phasic to that of neurons. Astrocytes release 'gliotransmitters', including glutamate, in response to an increase in [Ca2+]i. When the authors expressed a genetically encoded sensor of the extracellular glutamate concentration ([Glu]e) in SCN slices, they observed circadian oscillations in [Glu]e that were in phase with astrocytic [Ca2+]i. oscillations. That astrocytes were the source of the measured [Glu]e was supported by the fact that the pharmacological inhibition of astrocytic glutamate catabolism or the genetic ablation of astrocytes, respectively, increased or reduced [Glu]e. © 2017 Macmillan Publishers Limited,

Keyword: Biological Rhythms; Glia
Link ID: 23436 - Posted: 04.01.2017

By KATIE THOMAS The Food and Drug Administration approved on Tuesday the first drug to treat a severe form of multiple sclerosis, offering hope to patients who previously had no other options to combat a relentless disease that leads to paralysis and cognitive decline. The federal agency also cleared the drug to treat people with the more common, relapsing form of the disease. “I think that this is a very big deal,” said Dr. Stephen Hauser, the chairman of the neurology department at the University of California, San Francisco, and leader of the steering committee that oversaw the late-stage clinical trials of the drug, ocrelizumab. “The magnitude of the benefits that we’ve seen with ocrelizumab in all forms of M.S. are really quite stunning.” The drug, which will be sold under the brand name Ocrevus by Genentech, showed the most notable results in patients with relapsing multiple sclerosis, appearing to halt progression of the disease with few serious side effects. In patients with the more severe form, primary progressive multiple sclerosis, the drug only modestly slowed patients’ decline, but medical experts described it as an important first step. “This sort of opens the door for us,” said Dr. Fred D. Lublin, who was a crucial investigator for the clinical trial and is director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at Mount Sinai Hospital in New York. “Once we open that door, then we do better and better and better. It’s a very encouraging result.” Genentech, which is owned by the Swiss pharmaceutical giant Roche, said Tuesday that it would charge a list price of $65,000 a year, which — though expensive — is 25 percent less than an existing drug, Rebif, that was shown to be clinically inferior to Ocrevus in the two clinical trials that led to Ocrevus’s approval. © 2017 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 23421 - Posted: 03.29.2017

By Erik Vance The world’s smallest arachnid, the Samoan moss spider, is at a third of a millimeter nearly invisible to the human eye. The largest spider in the world is the goliath birdeater tarantula, which weighs 5 ounces and is about the size of a dinner plate. For reference, that is about the same difference in scale between that same tarantula and a bottlenose dolphin. And yet the bigger spider does not act in more complex ways than its tiny counterpart. “Insects and spiders and the like—in terms of absolute size—have among the tiniest brains we’ve come across,” says William Wcislo, a scientist at the Smithsonian Tropical Research Institute in Panama City. “But their behavior, as far as we can see, is as sophisticated as things that have relatively large brains. So then there’s the question: How do they do that?” No one would argue that a tarantula is as smart as a dolphin or having a really big brain is not an excellent way to perform complicated tasks. But a growing number of scientists are asking the question: Is it the only way? Do you need a big brain to hunt elusive prey, design complicated structures or produce complex social dynamics? For generations scientists have wondered how intelligent creatures developed large brains to perform complicated tasks. But Wcislo is part of a small community of scientists less interested in how brains have grown than how they have shrunk and yet shockingly still perform tasks as well or better than similar species that are much larger in size. In other words, it’s what scientists call brain miniaturization, not unlike the scaling down in size of the transistors in a computer chip. This research, in fact, may hold clues to innovative design strategies that engineers might incorporate in future generations of computers. © 2017 Scientific American

Keyword: Miscellaneous
Link ID: 23418 - Posted: 03.29.2017