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

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A small group of cells in the brain can have a big effect on seizures and memory in a mouse model of epilepsy. According to a new study in Science, loss of mossy cells may contribute to convulsive seizures in temporal lobe epilepsy (TLE) as well as memory problems often experienced by people with the disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The role of mossy cells in epilepsy has been debated for decades. This study reveals how critical these cells are in the disease, and the findings suggest that preventing loss of mossy cells or finding ways to activate them may be potential therapeutic targets,” said Vicky Whittemore, Ph.D., program director at NINDS. Mossy cells, named for the dense moss-like protrusions that cover their surface, are located in the hippocampus, a brain area that is known to play key roles in memory. Loss of mossy cells is associated with TLE, but it is unknown what role that plays in the disease. Using state-of-the-art tools, Ivan Soltesz, Ph.D., professor of neurosurgery and neurosciences at Stanford University, Palo Alto, California, and his team were able to turn mossy cells on and off to track their effects in a mouse model of epilepsy. “This study would not have been possible without the rapid advancement of technology, thanks in part to the BRAIN Initiative, which has encouraged scientists to develop innovative instruments and new ways to look at the brain,” said Dr. Soltesz. “It’s remarkable that we can manipulate specific brain cells in the hippocampus of a mouse. Using 21st century tools brings us closer than ever to unlocking the mysteries behind this debilitating disease.”

Keyword: Epilepsy; Learning & Memory
Link ID: 24669 - Posted: 02.16.2018

By Diana Kwon When optogenetics debuted over a decade ago, it quickly became the method of choice for many neuroscientists. By using light to selectively control ion channels on neurons in living animal brains, researchers could see how manipulating specific neural circuits altered behavior in real time. Since then, scientists have used the technique to study brain circuity and function across a variety of species, from fruit flies to monkeys—the method is even being tested in a clinical trial to restore vision in patients with a rare genetic disorder. Today (February 8) in Science, researchers report successfully conducting optogenetics experiments using injected nanoparticles in mice, inching the field closer to a noninvasive method of stimulating the brain with light that could one day have therapeutic uses. “Optogenetics revolutionized how we all do experimental neuroscience in terms of exploring circuits,” says Thomas McHugh, a neuroscientist at the RIKEN Brain Science Institute in Japan. However, this technique currently requires a permanently implanted fiber—so over the last few years, researchers have started to develop ways to stimulate the brain in less invasive ways. A number of groups devised such techniques using magnetic fields, electric currents, and sound. McHugh and his colleagues decided to try another approach: They chose near-infrared light, which can more easily penetrate tissue than the blue-green light typically used for optogenetics. “What we saw as an advantage was a kind of chemistry-based approach in which we can harness the power of near-infrared light to penetrate tissue, but still use this existing toolbox that's been developed over the last decade of optogenetic channels that respond to visible light,” McHugh says. © 1986-2018 The Scientist

Keyword: Brain imaging
Link ID: 24637 - Posted: 02.09.2018

By Helen Shen Noninvasive brain stimulation is having its heyday, as scientists and hobbyists alike look for ways to change the activity of neurons without cutting into the brain and implanting electrodes. One popular set of techniques, called transcranial electrical stimulation (TES), delivers electrical current via electrodes stuck to the scalp, typically above the target brain area. In recent years a number of studies have attributed wide-ranging benefits to TES including enhancing memory, improving math skills, alleviating depression and even speeding recovery from stroke. Such results have also spawned a cottage industry providing commercial TES kits for DIY brain hackers seeking to boost their mind power. But little is known about how TES actually interacts with the brain, and some studies have raised serious doubts about the effectiveness of these techniques. A study published on February 2 in Nature Communications ups the ante, reporting that conventional TES techniques do not deliver enough current to activate brain circuits or modulate brain rhythms. The electrical currents mostly fizzle out as they pass through the scalp and skull. “Anybody who has published a positive effect in this field is probably not going to like our paper,” says György Buzsáki, a neuroscientist at New York University and a senior author of the study. The mechanisms behind TES have remained mysterious, in part because without penetrating the skull, researchers cannot measure neural responses while they apply stimulation. Conventional TES methods produce electrical noise that swamps any brain activity detected on the scalp. © 2018 Scientific American

Keyword: Learning & Memory
Link ID: 24622 - Posted: 02.06.2018

Jon Hamilton When Sarah Jay had her first seizure, she was in her mid-20s and working a high-stress job at a call center in Springfield, Mo. "I was going to go on break," she says. "I was heading towards the bathroom and then I fell and passed out." An ambulance took Jay to the hospital but doctors there couldn't find anything wrong. Jay figured it was a one-time thing. Then a week later, she had another seizure. And that kept happening once or twice a week. "So I was put on short-term disability for my work to try to figure out what was going on," says Jay, who's now 29. The most likely cause for her seizures was abnormal electrical activity in her brain. In other words, epilepsy. But Jay's doctors wanted to be sure. In May 2013, they admitted her to a hospital epilepsy center, put electrodes on her scalp and began watching her brain activity. An epileptic seizure looks a bit like an electrical storm in the brain. Neurons begin to fire uncontrollably, which can cause patients to lose consciousness or have muscle spasms. But during Jay's seizures, her brain activity appeared completely normal. "It was kind of surreal," she says. "This woman, she sat me down and she was like, 'OK, you do not have epilepsy.' And I'm like, 'OK, so what's going on?' " The woman told Jay her seizures were the result of a psychological disorder called psychogenic non-epileptic seizures. PNES is a surprisingly common disorder, says John Stern, who directs the epilepsy clinical program at the University of California, Los Angeles. About 1 in 3 people who come to UCLA for uncontrolled seizures don't have epilepsy. Usually, they have PNES, he says. © 2018 npr

Keyword: Epilepsy; Stress
Link ID: 24606 - Posted: 02.02.2018

Sara Reardon Superconducting computing chips modelled after neurons can process information faster and more efficiently than the human brain. That achievement, described in Science Advances on 26 January1, is a key benchmark in the development of advanced computing devices designed to mimic biological systems. And it could open the door to more natural machine-learning software, although many hurdles remain before it could be used commercially. Artificial intelligence software has increasingly begun to imitate the brain. Algorithms such as Google’s automatic image-classification and language-learning programs use networks of artificial neurons to perform complex tasks. But because conventional computer hardware was not designed to run brain-like algorithms, these machine-learning tasks require orders of magnitude more computing power than the human brain does. “There must be a better way to do this, because nature has figured out a better way to do this,” says Michael Schneider, a physicist at the US National Institute of Standards and Technology (NIST) in Boulder, Colorado, and a co-author of the study. NIST is one of a handful of groups trying to develop ‘neuromorphic’ hardware that mimics the human brain in the hope that it will run brain-like software more efficiently. In conventional electronic systems, transistors process information at regular intervals and in precise amounts — either 1 or 0 bits. But neuromorphic devices can accumulate small amounts of information from multiple sources, alter it to produce a different type of signal and fire a burst of electricity only when needed — just as biological neurons do. As a result, neuromorphic devices require less energy to run. © 2018 Macmillan Publishers Limited

Keyword: Robotics; Learning & Memory
Link ID: 24579 - Posted: 01.27.2018

By Eli Meixler Friday’s Google Doodle celebrates the birthday of Wilder Penfield, a scientist and physician whose groundbreaking contributions to neuroscience earned him the designation “the greatest living Canadian.” Penfield would have turned 127 today. Later celebrated as a pioneering researcher and a humane clinical practitioner, Penfield pursued medicine at Princeton University, believing it to be “the best way to make the world a better place in which to live.” He was drawn to the field of brain surgery, studying neuropathy as a Rhodes scholar at Oxford University. In 1928, Penfield was recruited by McGill University in Montreal, where he also practiced at Royal Victoria Hospital as the city’s first neurosurgeon. Penfield founded the Montreal Neurological Institute with support from the Rockefeller Foundation in 1934, the same year he became a Canadian citizen. Penfield pioneered a treatment for epilepsy that allowed patients to remain fully conscious while a surgeon used electric probes to pinpoint areas of the brain responsible for setting off seizures. The experimental method became known as the Montreal Procedure, and was widely adopted. But Wilder Penfield’s research led him to another discovery: that physical areas of the brain were associated with different duties, such as speech or movement, and stimulating them could generate specific reactions — including, famously, conjuring a memory of the smell of burnt toast. Friday’s animated Google Doodle features an illustrated brain and burning toast. © 2017 Time Inc.

Keyword: Miscellaneous
Link ID: 24576 - Posted: 01.27.2018

by Ariana Eunjung Cha A new class of epilepsy medications based on an ingredient derived from marijuana could be available as soon as the second half of 2018 in the United States, pending Food and Drug Administration approval. Officials from GW Pharmaceuticals, the company that developed the drug, on Wednesday announced promising results from a study on 171 patients randomized into treatment and placebo groups. Members of the group, ages 2 to 55, have a condition called Lennox-Gastaut syndrome and were suffering from seizures that were not being controlled by existing drugs. On average they had tried and discontinued six anti-seizure treatments and were experiencing 74 “drop” seizures per month. Drop seizures involve the entire body, trunk or head and often result in a fall or other type of injury. The results, published in the Lancet, show that over a 14-week treatment period, 44 percent of patients taking the drug, called Epidiolex, saw a significant reduction in seizures, compared with 22 percent of the placebo group. Moreover, more of the patients who got the drug experienced a 50 percent or greater reduction in drop seizures. Elizabeth Thiele, director of pediatric epilepsy at Massachusetts General Hospital and lead author of the study, said the results varied depending on the patient. “For some, it does not do a whole lot. But for the people it does work in, it is priceless,” she said. “One child who comes to mind had multiple seizures a day. She had been on every medication possible,” said Thiele, a professor of neurology at Harvard Medical School. Then the patient tried the cannabis-based treatment and has been seizure-free for almost four years. “She is now talking about college options. She would have never had that conversation before. It has been life-changing.” © 1996-2018 The Washington Post

Keyword: Epilepsy; Drug Abuse
Link ID: 24573 - Posted: 01.26.2018

By Diana Kwon Centuries ago, humans believed that seizures were tied to the lunar cycle. Although scientific evidence for this association is scarce, physicians have long suspected that temporal patterns connected with epilepsy may exist. These days, the condition’s link to our sleep-wake cycles, or circadian rhythms, is well-documented, primarily through observations that seizures are more prevalent at night or tend to occur at specific times of day. Scientists now report the existence of seizure-associated brain rhythms with longer periods, most commonly within the 20- to 30-day range, in a study published today (January 8) in Nature Communications. “People have made these observations since antiquity and have wanted to speculate and explain these oscillations for a long time,” study coauthor Vikram Rao, a neurologist at the University of California, San Francisco, tells The Scientist. “But only recently [have we gotten] the tools that might allow us to actually unravel this.” Rao and his colleagues analyzed data collected from one such tool—the NeuroPace device, an FDA-approved, implanted brain stimulator that continuously monitors neural activity and sends electrical pulses when a seizure is imminent. It acts, in some sense, like a “pacemaker for the brain,” Rao says. The device detects and records both seizures and interictal epileptiform discharges, pathological brain activity associated with these events, using electroencephalography (EEG). “In between seizures, we see electric discharges that signify irritability of the brain and a propensity to have seizures,” Rao explains. “It’s like seeing sparks from a match, where you say, wow, that looks like there’s potential for a fire but it’s not the fire itself.” © 1986-2018 The Scientist

Keyword: Epilepsy; Biological Rhythms
Link ID: 24513 - Posted: 01.10.2018

By Kasra Zarei Depression and antidepressant use are at all-time highs in the year 2017, but for about a third of those affected, depression still doesn’t get better with medication—and for these patients, transcranial magnetic stimulation (TMS), which uses powerful magnets to stimulate brain cells noninvasively, can be a viable option. To be clear, TMS isn’t new; it was first approved by the FDA in 2008. What’s new is that the evidence for its safety and effectiveness has only gotten stronger. TMS is now generally covered by insurance companies for treatment-resistant depression, and new studies have shown that combining it with traditional treatments like psychotherapy can lead to significantly higher response rates. Some scientists also now believe TMS can be a dominant therapy compared to antidepressants, based on its lower cost, higher net monetary benefit and better quality of life outcomes produced. Although there are still many questions about TMS left unanswered, it is a treatment with a strong presence in fighting depression and much promise as personalized TMS grows closer to becoming a reality. According to the World Health Organization, an estimated 350 million people worldwide suffer from depression, making it the leading cause of disability worldwide. As many as 30 percent of people with depression are resistant to medication, and show suicide thoughts and attempts, and an overall poor quality of life. With traditional treatment options ineffective, these patients need a solution. © 2017 Scientific American

Keyword: Depression
Link ID: 24447 - Posted: 12.21.2017

By Roni Dengler Our brains don’t rest when we sleep. Electrical waves ripple through our noggins as our neurons talk to each other. Now, researchers have shown that when these waves don’t interact properly, we can lose our long-term memory. The work may help explain why older adults are so forgetful, and it could lead to new therapies to treat memory loss. To find out how sleep contributes to memory loss in old age, Randolph Helfrich, a neuroscientist at the University of California (UC), Berkeley, and his team gave healthy 70- and 20-year-olds a memory test. Participants were trained to match 120 common, short words—for example, “bird”—with nonsense words made of combinations of random syllables, like “jubu.” Once they learned the word-nonsense word combos, the volunteers played a version of the game “memory.” They had to match the word pairs twice: once about 10 minutes after they’d mastered the task, and again a few hours after waking from a full night’s rest. While they slept, researchers recorded the electrical activity in their brains. As expected, the older adults’ ability to remember the word pairs in the morning was worse than their young counterparts’. The electrical recordings revealed one reason. Two kinds of brain waves—slow oscillations, large undulations that promote restorative sleep, and sleep spindles, transient bursts of short waves—are tell-tale marks of deep, typically dreamless, non–rapid eye movement sleep. But these waves are out of sync in older people, the researchers report today in Neuron. This out-of-step activity, they say, interrupts communication between the parts of our brains that store short- and long-term memories. In effect, Helfrich says, the prefrontal cortex where long-term memories are stored needs to tell the hippocampus—the part of the brain where all memories go first—that it’s ready to receive information; if brain waves aren’t in sync, this communication gets lost. So do the memories. © 2017 American Association for the Advancement of Science

Keyword: Learning & Memory; Alzheimers
Link ID: 24428 - Posted: 12.15.2017

By Helen Branswell, What many hope will be the final chapter in an unfortunate saga in multiple sclerosis research appears to have been written by the scientist who started the affair in the first place. Italian physician Paolo Zamboni has publicly acknowledged that a therapy he developed and dubbed “the liberation treatment” does not cure or mitigate the symptoms of MS. A randomized controlled trial—the gold standard of medical research—he and other Italian researchers conducted concluded the procedure is a “largely ineffective technique” that should not be recommended for MS patients. The trial’s result comes as no surprise to neurologists, most of whom felt Zamboni’s theory lacked plausibility from the moment news of it exploded through the MS community in 2009. Advertisement Many of those same neurologists, though, saw their relationships with their patients fractured as belief in the liberation therapy took hold in the community of patients and their families in Canada, parts of the United States, and farther afield. Doctors advising caution against a procedure that hadn’t been proved to work or even to be safe were derided as standing in the way of innovation to protect their own practices. Dr. Jock Murray, an MS expert and retired professor from Dalhousie University in Halifax, Nova Scotia, said the history of MS is laden with incidences like the Zamboni episode—though he said this one lasted longer than most. © 2017 Scientific American,

Keyword: Multiple Sclerosis
Link ID: 24378 - Posted: 11.30.2017

Summary A vast effort by a team of Janelia Research Campus scientists is rapidly increasing the number of fully-traced neurons in the mouse brain. Researchers everywhere can now browse and download the 3-D data. Inside the mouse brain, individual neurons zigzag across hemispheres, embroider branching patterns, and, researchers have now shown, often spool out spindly fibers nearly half a meter long. Scientists can see and explore these wandering neural traces in 3-D, in the most extensive map of mouse brain wiring yet attempted. The map – the result of an ongoing effort by an eclectic team of researchers at the Janelia Research Campus – reconstructs the entire shape and position of more than 300 of the roughly 70 million neurons in the mouse brain. Previous efforts to trace the path of individual neurons had topped out in the dozens. “Three hundred neurons is just the start,” says neuroscientist Jayaram Chandrashekar, who leads the Janelia project team, called MouseLight for its work illuminating the circuitry of the mouse brain. He and colleagues expect to trace hundreds more neurons in the coming months – and they’re sharing all the data with the neuroscience community. The team released their current dataset and an analysis tool, called the MouseLight NeuronBrowser, on October 27, 2017, and will report the work in November at the annual Society for Neuroscience meeting in Washington, D.C. They hope that the findings will help scientists ask, and begin to answer, questions about how neurons are organized, and how information flows through the brain. ©2017 Howard Hughes Medical Institute

Keyword: Brain imaging
Link ID: 24319 - Posted: 11.11.2017

Laura Sanders The human brain is teeming with diversity. By plucking out delicate, live tissue during neurosurgery and then studying the resident cells, researchers have revealed a partial cast of neural characters that give rise to our thoughts, dreams and memories. So far, researchers with the Allen Institute for Brain Science in Seattle have described the intricate shapes and electrical properties of about 100 nerve cells, or neurons, taken from the brains of 36 patients as they underwent surgery for conditions such as brain tumors or epilepsy. To reach the right spot, surgeons had to remove a small hunk of brain tissue, which is usually discarded as medical waste. In this case, the brain tissue was promptly packed up and sent — alive — to the researchers. Once there, the human tissue was kept on life support for several days as researchers analyzed the cells’ shape and function. Some neurons underwent detailed microscopy, which revealed intricate branching structures and a wide array of shapes. The cells also underwent tiny zaps of electricity, which allowed researchers to see how the neurons might have communicated with other nerve cells in the brain. The Allen Institute released the first publicly available database of these neurons on October 25. A neuron called a pyramidal cell, for instance, has a bushy branch of dendrites (orange in 3-D computer reconstruction, above) reaching up from its cell body (white circle). Those dendrites collect signals from other neural neighbors. Other dendrites (red) branch out below. The cell’s axon (blue) sends signals to other cells that spur them to action. |© Society for Science & the Public 2000 - 2017.

Keyword: Brain imaging
Link ID: 24314 - Posted: 11.10.2017

Megan Molteni For patients with epilepsy, or cancerous brain lesions, sometimes the only way to forward is down. Down past the scalp and into the skull, down through healthy grey matter to get at a tumor or the overactive network causing seizures. At the end of the surgery, all that extra white and grey matter gets tossed in the trash or an incinerator. Well, not all of it. At least, not in Seattle. For the last few years, doctors at a number of hospitals in the Emerald City have been saving those little bits and blobs of brain, sticking them on ice, and rushing them off in a white van across town to the Allen Institute for Brain Science. Scientists there have been keeping the tissue on life support long enough to tease out how individual neurons look, act, and communicate. And today they’re sharing the first peek at these cells in a freely available public database. It provides a more intimate, intricate look into the circuitry of the human brain than ever before. And it’s just the beginning of a much larger effort to build a complete catalog of human brain cells. This first release includes electrical readings from a few hundred living neurons—all recently removed from 36 neurosurgery patients in Seattle area hospitals. For 100 of those cells, Allen Institute researchers built 3-D models of their branching structures, which they can use to simulate patterns of pulses and zaps. Scientists can see where in the brain neurons start and stop, and how current flows and spreads a signal throughout a neuronal network—signals that might move a muscle, or make a memory.

Keyword: Brain imaging
Link ID: 24245 - Posted: 10.26.2017

By GRETCHEN REYNOLDS Here’s yet another reason to protect young athletes from head trauma: A large-scale new study found that concussions in adolescents can increase the risk of later developing multiple sclerosis. The risk of multiple sclerosis, or M.S., an autoimmune nervous system disorder with an unknown cause, was especially high if there were more than one head injury. The overall chances that a young athlete who has had one or more head injuries will develop multiple sclerosis still remain low, the study’s authors point out. But the risk is significantly higher than if a young person never experiences a serious blow to the head. The drumbeat of worrying news about concussions and their consequences has been rising in recent years, as most of us know, especially if we have children who play contact sports. Much of this concern has centered on possible links between repeated concussions and chronic traumatic encephalopathy, a serious, degenerative brain disease that affects the ability to think. But there have been hints that head trauma might also be linked to the development of other conditions, including multiple sclerosis. Past studies with animals have shown that trauma to the central nervous system, including the brain, may jump-start the kind of autoimmune reactions that underlie multiple sclerosis. (In the disease, the body’s immune system begins to attack the fatty sheaths that enwrap and protect nerve fibers, leaving them vulnerable to damage and scarring.) © 2017 The New York Times Company

Keyword: Brain Injury/Concussion; Multiple Sclerosis
Link ID: 24219 - Posted: 10.19.2017

By Sara Van Note On a recent Saturday morning, two-year-old Ryleigh and five-year-old Colton Arnett play with brightly colored play dough in the family room of their Albuquerque home. Colton narrates his creations with a gap-toothed smile. “I’m going to use a mold. I’m going to make a boat.” Ryleigh echoes him enthusiastically, “Mold! Boat!” An estimated 30,000 New Mexicans carry the mutation, and the numbers are increasing. Their mother, Lori Dunworth, remarks that Colton and his sister don’t usually play so well together. “Usually she’s a bit of a bully when it comes to toys.” Both Ryleigh and Colton receive speech therapy because of something that happened to Colton several years ago, when Dunworth and her husband, Toby Arnett, first noticed that Colton, who was two at the time, was making repeating clicking sounds while his face twitched on one side. After one episode lasted over 20 minutes, they called their doctor, who told them to take him to the hospital immediately. Colton had suffered a seizure, and scans would later reveal masses in his brain — lesions, it turned out, caused by abnormal blood vessels. “The original impact was devastating,” Arnett says. Colton was ultimately diagnosed with Cerebral Cavernous Malformations (CCM), a rare disease that can cause seizure, stroke, and death. He also tested positive for a genetic mutation that causes the disease, known as the Common Hispanic Mutation. Colton’s sister and his mom also have the mutation. Dunworth had no idea she was the carrier. “I’ve never had any symptoms, no seizures, no paralysis, no nothing,” she says. Copyright 2017 Undark

Keyword: Epilepsy; Genes & Behavior
Link ID: 24184 - Posted: 10.12.2017

By Dan Stark I used to tell people considering deep brain stimulation — which involves the surgical implantation of electrodes into the brain — that it gave the typical Parkinson’s sufferer perhaps 10 years of relief, during which the symptoms would be relatively minor. The bet — this is, after all, brain surgery that carries some risk of serious adverse results — would be that sometime during that decade, researchers would come up with a real solution. In other words, DBS was a way to buy time. Still, 10 years is no small period, particularly for those who have no other hope. My experience is typical. I had DBS just under 12 years ago. Things went so well that I became a huge fan of the procedure. But DBS works on only some Parkinson’s symptoms. (Drooling, for example, is not affected.) For slightly more than a decade, DBS performed wonders on me, eliminating the shakes that had accompanied my attempts to beat back Parkinson’s symptoms with medicine alone. But because DBS masks the symptoms while not affecting the underlying disease, in the end it will fail the Parkinson’s patient. For me, the failure was in the form of a one-two punch. The first blow was self-inflicted. In April, one of the batteries powering my neural implants died. That was my fault; one should monitor the batteries and replace them in advance. Because I hadn’t, I got a taste of what life would be like without the stimulators. © 1996-2017 The Washington Post

Keyword: Parkinsons
Link ID: 24132 - Posted: 10.02.2017

By John Horgan “The Forgotten Era of Brain Chips,” published in Scientific American in October 2005, has provoked as much interest as anything I’ve ever written. It focuses on Jose Manuel Rodriguez Delgado, a pioneer in brain-stimulation research. I keep hearing from journalists and others wanting more information on Delgado, whom I interviewed in 2005 and who died in 2011. Delgado fascinates conspiracy theorists, too. An article on Infowars.com describes him as a “madman” who believed that “no human being has an inherent right to his own personality.” Given widespread interest in and misinformation about Delgado, whose work prefigures current research on brain implants (see “Further Reading”), I’m posting an edited version of my 2005 article. --John Horgan Once among the world’s most acclaimed scientists, Jose Manuel Rodriguez Delgado has become an urban legend, whose career is shrouded in misinformation. Delgado pioneered that most unnerving of technologies, the brain chip, which manipulates the mind by electrically stimulating neural tissue with implanted electrodes. Long a McGuffin of science fictions, from The Terminal Man to The Matrix, brain chips are now being tested as treatments for epilepsy, Parkinson’s disease, paralysis, depression, and other disorders. In part because it was relatively unencumbered by ethical regulations, Delgado’s research rivaled and even surpassed much of what is being done today. In 1965, The New York Times reported on its front page that he had stopped a charging bull in its tracks by sending a radio signal to a device implanted in its brain. He also implanted radio-equipped electrode arrays, which he called “stimoceivers,” in dogs, cats, monkeys, chimpanzees, gibbons, and humans. With the push of a button, he could evoke smiles, snarls, bliss, terror, hunger, garrulousness, lust, and other responses. © 2017 Scientific American,

Keyword: Aggression
Link ID: 24131 - Posted: 10.02.2017

Mariah Quintanilla Kenneth Catania knows just how much it hurts to be zapped by an electric eel. For the first time, the biologist at Vanderbilt University in Nashville has measured the strength of a defensive electrical attack on a real-life potential predator — himself. Catania placed his arm in a tank with a 40-centimeter-long electric eel (relatively small as eels go) and determined, in amperes, the electrical current that flowed into him when the eel struck. At its peak, the current reached 40 to 50 milliamperes in his arm, he reports online September 14 in Current Biology. This zap was painful enough to cause him to jerk his hand from the tank during each trial. “If you’ve ever been on a farm and touched an electric fence, it’s pretty similar to that,” he says. This is Catania’s latest study in a body of research analyzing the intricacies of an electric eel’s behavior. The way electric eels have been described by biologists in the past has been fairly primitive, says Jason Gallant, a biologist who heads the Michigan State University Electric Fish Lab in East Lansing who was not involved in the study. Catania’s work reveals that “what the electric eel is doing is taking the electric ability that it has and using that to its absolute advantage in a very sophisticated, deliberate way,” he says. Electric eels use electric current to navigate, communicate and hunt for small prey. But when faced with a large land-based predator, eels will launch themselves from the water and electrify the animal with a touch of the head. |© Society for Science & the Public 2000 - 2017.

Keyword: Aggression
Link ID: 24068 - Posted: 09.15.2017

By Giorgia Guglielmi The trillions of bacteria that live in our intestines, known collectively as the gut microbiome, have been linked to maladies from eye disease to rheumatoid arthritis. Now, two new studies have added another disease: multiple sclerosis (MS), an autoimmune disorder that strips away nerve cells’ protective covers, leading to muscle weakness, blindness, and even death. What’s more, the studies suggest how our gut microbes make the immune system turn against nerve cells—a finding that could lead to treatments, like drugs based on microbial byproducts, that might improve the course of the disease. MS affects 2.5 million people worldwide, but little is known about what causes the disease, which progressively disrupts information flow from and within the brain. Most researchers think it starts when genetically predisposed people encounter an as-yet-unknown environmental trigger. Previous studies have identified particular bacteria present in increased amounts in the guts of MS patients. But the new papers “took it to the next level” in trying to understand how these bacteria affect the immune system, says Francisco Quintana, a neuroimmunologist at Brigham and Women’s Hospital in Boston not involved with the work. “These are going to be landmark studies.” In the first paper, a team of researchers led by Sergio Baranzini, a human geneticist at the University of California, San Francisco, analyzed the microbiomes of 71 people with MS and 71 healthy individuals, aged 19 to 71. They found that two bacterial groups, Acinetobacter and Akkermansia, were four times more abundant in MS patients than in individuals with no disease. Another group, Parabacteroides, was four times as abundant in healthy people. © 2017 American Association for the Advancement of Science

Keyword: Multiple Sclerosis
Link ID: 24059 - Posted: 09.13.2017