Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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Laura Sanders Flickering light kicks off brain waves that clean a protein related to Alzheimer’s disease out of mice’s brains, a new study shows. The results, described online December 7 in Nature, suggest a fundamentally new approach to counteracting Alzheimer’s. Many potential therapies involve drugs that target amyloid-beta, the sticky protein that accumulates in the brains of Alzheimer’s patients. In contrast, the new method used on mice causes certain nerve cells to fire at a specific rhythm, generating brain waves that researchers believe may clear A-beta. “This is a very creative and innovative new approach to targeting brain amyloid load in Alzheimer’s,” says geriatric psychiatrist Paul Rosenberg of Johns Hopkins Medicine. But he cautions that the mouse results are preliminary. Neuroscientist Li-Huei Tsai of MIT and colleagues saw that mice engineered to produce lots of A-beta don’t produce as many gamma waves in the hippocampus, a brain structure important for memory. Using a method called optogenetics, the researchers genetically designed certain nerve cells in the hippocampus to fire off signals in response to light. In this way, the researchers induced gamma waves — rhythmic firings 40 times per second. After just an hour of forced gamma waves, the mice had less A-beta in the hippocampus, the researchers found. Further experiments revealed that gamma waves packed a double whammy — they lowered A-beta by both reducing production and enhancing the brain’s ability to clear it. © Society for Science & the Public 2000 - 2016
Link ID: 22966 - Posted: 12.08.2016
Sara Reardon A new technique might allow researchers and clinicians to stimulate deep regions of the brain, such as those involved in memory and emotion, without opening up a patient’s skull. Brain-stimulation techniques that apply electrodes to a person’s scalp seem to be safe, and proponents say that the method can improve some brain functions, including enhancing intelligence and relieving depression. Some of these claims are much better supported by research than others. But such techniques are limited because they cannot reach deep regions of the brain. By contrast, implants used in deep brain stimulation (DBS) are much more successful at altering the inner brain. The devices can be risky, however, because they involve surgery, and the implants cannot be repaired easily if they malfunction. At the annual Society for Neuroscience conference, held in San Diego, California, last week, neuroengineer Nir Grossman of the Massachusetts Institute of Technology in Cambridge and his colleagues presented their experimental method that adapts transcranial stimulation (TCS) for the deep brain. Their approach involves sending electrical signals through the brain from electrodes placed on the scalp and manipulating the electrical currents in a way that negates the need for surgery. The team used a stimulation device to apply two electric currents to the mouse's skull behind its ears and tuned them to slightly different high frequencies. They angled these two independent currents so that they intersected with each other at the hippocampus. © 2016 Macmillan Publishers Limited,
By Clare Wilson It’s one of the boldest treatments in medicine: delivering an electrical current deep into the brain by implanting a long thin electrode through a hole in the skull. Such “deep brain stimulation” (DBS) works miracles on people with otherwise untreatable epilepsy or Parkinson’s disease – but drilling into someone’s head is an extreme step. In future, we may be able to get the same effects by using stimulators placed outside the head, an advance that could see DBS used to treat a much wider range of conditions. DBS is being investigated for depression, obesity and obsessive compulsive disorder, but this research is going slowly. Implanting an electrode requires brain surgery, and carries a risk of infection, so the approach is only considered for severe cases. But Nir Grossman of Imperial College London and his team have found a safer way to experiment with DBS – by stimulating the brain externally, with no need for surgery. The technique, unveiled at the Society for Neuroscience conference in San Diego, California, this week, places two electrical fields of different frequencies outside the head. The brain tissue where the fields overlap is stimulated, while the tissue under just one field is unaffected because the frequencies are too high. For instance, they may use one field at 10,000 hertz and another at 10,010 hertz. The affected nerve cells are stimulated at 10 hertz – the difference between the two frequencies. © Copyright Reed Business Information Ltd.
Link ID: 22875 - Posted: 11.16.2016
By Alison F. Takemura In the mid-1980s, György Buzsáki was trying to get inside rats’ heads. Working at the University of California, San Diego, he would anesthetize each animal with ether and hypothermia, cut through its scalp, and drill holes in its skull. Carefully, he’d screw 16 gold-plated stainless steel electrodes into the rat’s brain. When he was done with the surgery, these tiny pieces of metal—just 0.5 mm in diameter—allowed him to measure voltage changes from individual neurons deep in the brain’s folds, all while the rodent was awake and moving around. He could listen to the cells fire action potentials as the animal explored its environment, learning and remembering what it encountered (J Neurosci, 8:4007-26, 1988). In those days, recording from two cells simultaneously was the norm. The 16-site recording in Buzsáki’s 1988 study “was the largest ever in a rat,” he says. Nowadays, scientists can measure voltage changes from 1,000 neurons at the same time with silicon multielectrode arrays. But the basic techniques of using a probe to measure electrical activity within the brain (electrophysiology) or from outside it (electroencephalography, or EEG) are still workhorses of neural imaging labs. “The new tools don’t replace the old ones,” says Jessica Cardin, a neuroscientist at the Yale School of Medicine. “They add new layers of information.” Another decades-old neuroscientific technique that remains popular today is patch clamping. Developed in the late 1970s and early 1980s, it can detect changes in the electric potential of individual cells, or even single ion channels. With a tiny glass pipette suctioned against the cell’s membrane, researchers can make a small tear, sealed by the pipette tip, and detect voltage changes inside the cell. With some improvements, the patch clamp, like electrophysiology and EEG, has remained a regular part of the neuroscientist’s tool kit. Recently, researchers had a robot carry out the process (Nat Methods, 9:585-87, 2012). © 1986-2016 The Scientist
Keyword: Brain imaging
Link ID: 22783 - Posted: 10.25.2016
By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,
Link ID: 22754 - Posted: 10.13.2016
ByAnna Vlasits The next revolution in medicine just might come from a new lab technique that makes neurons sensitive to light. The technique, called optogenetics, is one of the biggest breakthroughs in neuroscience in decades. It has the potential to cure blindness, treat Parkinson’s disease, and relieve chronic pain. Moreover, it’s become widely used to probe the workings of animals’ brains in the lab, leading to breakthroughs in scientists’ understanding of things like sleep, addiction, and sensation. So it’s not surprising that the two Americans hailed as inventors of optogenetics are rock stars in the science world. Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology have collected tens of millions in grants and won millions in prize money in recent years. They’ve stocked their labs with the best equipment and the brightest minds. They’ve been lauded in the media and celebrated at conferences around the world. They’re considered all but certain to win a Nobel Prize. There’s only one problem with this story: It just may be that Zhuo-Hua Pan invented optogenetics first. Even many neuroscientists have never heard of Pan. Pan, 60, is a vision scientist at Wayne State University in Detroit who began his research career in his home country of China. He moved to the United States in the 1980s to pursue his PhD and never left. He wears wire-rimmed glasses over a broad nose framed by smile-lines in his cheeks. His colleagues describe him as a pure scientist: modest, dedicated, careful.
Keyword: Brain imaging
Link ID: 22625 - Posted: 09.03.2016
By GINA KOLATA Shena Pearson nearly froze in her seat, terrified, as she stared at a power-point slide. She was at her first meeting of an epilepsy foundation, seeking help for her 12-year-old son Trysten, when a neurologist flashed the slide about something called Sudep. It stands for sudden unexpected death in epilepsy. Her son’s neurologist had never mentioned it. “Oh dear God, my child is at risk, seriously at risk,” Ms. Pearson thought to herself. Sudden death in epilepsy is a little-known and seldom-mentioned phenomenon, but now, after a push by advocates, the federal government has begun a concerted program to understand it. Yet a question remains: When, if ever, should patients be warned? In a way, the extreme reticence of many neurologists to mention sudden unexpected death to epilepsy patients harks back to the days when doctors and families often did not tell people they had cancer — too terrifying. But today, patients learn not just about cancer but about many other potentially fatal conditions, like an inoperable brain aneurysm that could burst at any time and kill a person. So the quiet about the epilepsy death risk appears to be an anomaly. Sudep’s name pretty much explains what it is: Someone with epilepsy — unprovoked seizures, which are electrical surges in the brain — dies, and there is no apparent cause. Often a person with epilepsy goes to bed and is found in the morning, unresponsive. In some cases, there is indirect evidence of a seizure, like urine on the sheets, bloodshot eyes or a severely bitten tongue, leading to the suggestion that preventing seizures as much as possible with medications could lower patients’ risks. But so much about the syndrome remains unknown. © 2016 The New York Times Company
Link ID: 22587 - Posted: 08.23.2016
SINCE nobody really knows how brains work, those researching them must often resort to analogies. A common one is that a brain is a sort of squishy, imprecise, biological version of a digital computer. But analogies work both ways, and computer scientists have a long history of trying to improve their creations by taking ideas from biology. The trendy and rapidly developing branch of artificial intelligence known as “deep learning”, for instance, takes much of its inspiration from the way biological brains are put together. The general idea of building computers to resemble brains is called neuromorphic computing, a term coined by Carver Mead, a pioneering computer scientist, in the late 1980s. There are many attractions. Brains may be slow and error-prone, but they are also robust, adaptable and frugal. They excel at processing the sort of noisy, uncertain data that are common in the real world but which tend to give conventional electronic computers, with their prescriptive arithmetical approach, indigestion. The latest development in this area came on August 3rd, when a group of researchers led by Evangelos Eleftheriou at IBM’s research laboratory in Zurich announced, in a paper published in Nature Nanotechnology, that they had built a working, artificial version of a neuron. Neurons are the spindly, highly interconnected cells that do most of the heavy lifting in real brains. The idea of making artificial versions of them is not new. Dr Mead himself has experimented with using specially tuned transistors, the tiny electronic switches that form the basis of computers, to mimic some of their behaviour. © The Economist Newspaper Limited 2016.
By Simon Makin A technology with the potential to blur the boundaries between biology and electronics has just leaped a major hurdle in the race to demonstrate its feasibility. A team at the University of California, Berkeley, led by neuroscientist Jose Carmena and electrical and computer engineer Michel Maharbiz, has provided the first demonstration of what the researchers call “ultrasonic neural dust” to monitor neural activity in a live animal. They recorded activity in the sciatic nerve and a leg muscle of an anesthetized rat in response to electrical stimulation applied to its foot. “My lab has always worked on the boundary between biology and man-made things,” Maharbiz says. “We build tiny gadgets to interface synthetic stuff with biological stuff.” The work was published last week in the journal Neuron. The system uses ultrasound for both wireless communication and the device’s power source, eliminating both wires and batteries. It consists of an external transceiver and what the team calls a “dust mote” about 0.8x1x3 mm size, which is implanted inside the body. The transceiver sends ultrasonic pulses to a piezoelectric crystal in the implant, which converts them into electricity to provide power. The implant records electrical signals in the rat via electrodes, and uses this signal to alter the vibration of the crystal. These vibrations are reflected back to the transceiver, allowing the signal to be recorded—a technique known as backscatter. “This is the first time someone has used ultrasound as a method of powering and communicating with extremely small implantable systems,” says one of the paper’s authors, Dongjin Seo. “This opens up a host of applications in terms of embodied telemetry: being able to put something super-tiny, super-deep in the body, which you can park next to a nerve, organ, muscle or gastrointestinal tract, and read data out wirelessly.” © 2016 Scientific American
Keyword: Brain imaging
Link ID: 22533 - Posted: 08.09.2016
By James Gallagher Controlling human nerve cells with electricity could treat a range of diseases including arthritis, asthma and diabetes, a new company says. Galvani Bioelectronics hopes to bring a new treatment based on the technique before regulators within seven years. GlaxoSmithKline and Verily, formerly Google, Life Sciences, are behind it. Animal experiments have attached tiny silicone cuffs, containing electrodes, around a nerve and then used a power supply to control the nerve's messages. One set of tests suggested the approach could help treat type-2 diabetes, in which the body ignores the hormone insulin. They focused on a cluster of chemical sensors near the main artery in the neck that check levels of sugar and the hormone insulin. The sensors send their findings back to the brain, via a nerve, so the organ can coordinate the body's response to sugar in the bloodstream. GSK vice-president of bioelectronics Kris Famm told the BBC News website: "The neural signatures in the nerve increase in type 2-diabetes. "By blocking those neural signals in diabetic rats, you see the sensitivity of the body to insulin is restored." And early work suggested it could work in other diseases too. "It isn't just a one-trick-pony, it is something that if we get it right could have a new class of therapies on our hands," Mr Famm said. But he said the field was only "scratching the surface" when it came to understanding which nerve signals have what effect in the body. Both the volume and rhythm of the nerve signals could be having an effect rather than it being a simple case of turning the nerve on or off. © 2016 BBC
Link ID: 22507 - Posted: 08.03.2016
By Jessica Boddy Ever wonder what it looks like when brain cells chat up a storm? Researchers have found a way to watch the conversation in action without ever cracking open a skull. This glimpse into the brain’s communication system could open new doors to diagnosing and treating disorders from epilepsy to Alzheimer’s disease. Being able to see where—and how—living brain cells are working is “the holy grail in neuroscience,” says Howard Federoff, a neurologist at Georgetown University in Washington, D.C., who was not involved with the work. “This is a possible new tool that could bring us closer to that.” Neurons, which are only slightly longer than the width of a human hair, are laid out in the brain like a series of tangled highways. Signals must travel down these highways, but there’s a catch: The cells don’t actually touch. They’re separated by tiny gaps called synapses, where messages, with the assistance of electricity, jump from neuron to neuron to reach their destinations. The number of functional synapses that fire in one area—a measure known as synaptic density—tends to be a good way to figure out how healthy the brain is. Higher synaptic density means more signals are being sent successfully. If there are significant interruptions in large sections of the neuron highway, many signals may never reach their destinations, leading to disorders like Huntington disease. The only way to look at synaptic density in the brain, however, is to biopsy nonliving brain tissue. That means there’s no way for researchers to investigate how diseases like Alzheimer’s progress—something that could hold secrets to diagnosis and treatment. © 2016 American Association for the Advancement of Science
Keyword: Brain imaging
Link ID: 22472 - Posted: 07.23.2016
By ANNA WEXLER EARLIER this month, in the journal Annals of Neurology, four neuroscientists published an open letter to practitioners of do-it-yourself brain stimulation. These are people who stimulate their own brains with low levels of electricity, largely for purposes like improved memory or learning ability. The letter, which was signed by 39 other researchers, outlined what is known and unknown about the safety of such noninvasive brain stimulation, and asked users to give careful consideration to the risks. For the last three years, I have been studying D.I.Y. brain stimulators. Their conflict with neuroscientists offers a fascinating case study of what happens when experimental tools normally kept behind the closed doors of academia — in this case, transcranial direct current stimulation — are appropriated for use outside them. Neuroscientists began experimenting in earnest with transcranial direct current stimulation about 15 years ago. In such stimulation, electric current is administered at levels that are hundreds of times less than those used in electroconvulsive therapy. To date, more than 1,000 peer-reviewed studies of the technique have been published. Studies have suggested, among other things, that the stimulation may be beneficial for treating problems like depression and chronic pain as well as enhancing cognition and learning in healthy individuals. The device scientists use for stimulation is essentially a nine-volt battery attached to two wires that are connected to electrodes placed at various spots on the head. A crude version can be constructed with just a bit of electrical know-how. Consequently, as reports of the effects of the technique began to appear in scientific journals and in newspapers, people began to build their own devices at home. By late 2011 and early 2012, diagrams, schematics and videos began to appear online. © 2016 The New York Times Company
Link ID: 22471 - Posted: 07.23.2016
By Emma Bryce In 1999, neuroscientist Gero Miesenböck dreamed of using light to expose the brain's inner workings. Two years later, he invented optogenetics, a technique that fulfils this goal: by genetically engineering cells to contain proteins that make them light-responsive, Miesenböck found he could shine light at the brain and trigger electrical activity in those cells. This technique gave scientists the tools to activate and control specific cell populations in the brain, for the first time. For example, Miesenböck, who directs the Centre for Neural Circuits and Behaviour at the University of Oxford, first used optogenetics to activate courtship responses in fruit flies, and even make headless flies take flight - groundbreaking experiments that allowed him to examine, in unprecedented detail, how neurons drive behaviour. Gero Miesenböck: There was almost a "eureka" moment. As is often the case, you tend to have your best ideas when you're not trying to have them: suddenly I had this idea - which I must have been incubating for a long time, because I was thinking about manipulating neurons in the brain genetically to emit light so I could visualise their activity. Suddenly I thought, "What if we just turn the thing upside down, and instead of reading activity, write activity using light and genetics?" That was the real breakthrough idea, and then of course came the big challenge of having to make it work. Brains are composed of many different kinds of nerve cells, and they are genetically distinct from one another. To deconstruct how the brain works we need to pinpoint the roles these individual classes of cells play in processing information. Optogenetics uses the genetic signatures that define individual cell types to address them selectively in the intact brain - that's the "genetics" component. The "opto" component is to use these genetic signatures to place light-sensitive molecules that are encoded in DNA within these cells.
Link ID: 22469 - Posted: 07.23.2016
By Minaz Kerawala, For years, gamers, athletes and even regular people trying to improving their memory have resorted, with electrified enthusiasm, to "brain zapping" to gain an edge. The procedure, called transcranial direct current stimulation (tDCS), uses a battery and electrodes to deliver electrical pulses to the brain, usually through a cap or headset fitted close to the scalp. Proponents say these currents are beneficial for a range of neurological conditions like Alzheimer's and Parkinson's diseases, stroke and schizophrenia, but experts are warning that too little is known about the safety of tDCS. "You might end up with a placement of electrodes that doesn't do what you think it does and could potentially have long-lasting effects," said Matthew Krause, a neuroscientist at the Montreal Neurological Institute. All functions of the brain—thought, emotion and coordination—are carried out by neurons using pulses of electricity. "The objective of all neuroscience is to influence these electrical processes," Krause said. The brain's activity can be influenced by drugs that alter its electrochemistry or by external external electric fields. While mind-altering headsets may seem futuristic, tDCS is not a new procedure. Much of the pioneering work in the field was done in Montreal by Dr. Wilder Penfield in the 1920s and 30s. ©2016 CBC/Radio-Canada.
Link ID: 22464 - Posted: 07.21.2016
BBC journalist Caroline Wyatt has said she is determined to make the most of her life after being diagnosed with multiple sclerosis (MS). In her first interview since revealing the news last week, Wyatt told the Radio Times: "It is what it is." "I am not angry, and I don't want bitterness to start eating away at me." One of the best known faces of BBC News, Wyatt recently stepped down as the corporation's religious affairs correspondent due to her condition. 'Incredibly blessed' "I feel really sad now because I'm not going to be a correspondent full-time anymore - I physically can't." Wyatt had been struggling with undiagnosed symptoms for 25 years but was only diagnosed with MS last July after she was paralysed down her left side. Wyatt, who was also the BBC's defence correspondent, said she has had moments where she has questioned her own mortality. "Reporting news is often about reporting death, particularly in the places I have been. But it's less terrifying to me to think of being blown up and dying than to think 'gosh, I might decline slowly day by day, losing a little bit of capability every day'." At the moment, she is a bit unsteady on her feet and is struggling with her vision but still says she is "incredibly lucky and incredibly blessed". She is currently on a long summer break but is hoping to return to radio broadcasting later in the year, along with covering the canonisation of Mother Teresa in Rome. In MS the protective layer surrounding nerve fibres in the brain and spinal cord - known as myelin - becomes damaged. The immune system mistakenly attacks the myelin, causing scarring or sclerosis. The damaged myelin disrupts the nerve signals - rather like the short circuit caused by a frayed electrical cable. © 2016 BBC.
Keyword: Multiple Sclerosis
Link ID: 22341 - Posted: 06.21.2016
Aggressive chemotherapy followed by a stem cell transplant can halt the progression of multiple sclerosis (MS), a small study has suggested. The research, published in The Lancet, looked at 24 patients aged between 18 and 50 from three hospitals in Canada. For 23 patients the treatment greatly reduced the onset of the disease, but in one case a person died. An MS Society spokeswoman said this type of treatment does "offer hope" but also comes with "significant risks". Around 100,000 people in the UK have MS, which is an incurable neurological disease. 'No relapses' The condition causes the immune system to attack the lining of nerves in the brain and spinal cord. Most patients are diagnosed in their 20s and 30s. One existing treatment is for the immune system to be suppressed with chemotherapy and then stem cells are introduced to the patient's bloodstream - this procedure is known as an autologous haematopoietic stem cell transplant (HSCT). But in this study, Canadian researchers went further - not just suppressing the immune system, but destroying it altogether. It is then rebuilt with stem cells harvested from the patient's own blood which are at such an early stage, they have not developed the flaws that trigger MS. The authors said that among the survivors, over a period of up to 13 years, there were no relapses and no new detectable disease activity. All the patients who took part in the trial had a "poor prognosis" and had previously undergone standard immunosuppressive therapy which had not controlled the MS - which affects around two million people worldwide. © 2016 BBC.
By Rita Celli, This is what Jennifer Molson remembers doctors saying to her about the high-stakes procedure she would undergo in 2002 as part of an Ottawa study that has yielded some promising results in multiple sclerosis patients. The 41-year-old Ottawa woman was in a wheelchair before the treatment. She now walks, runs and works full time. "I had no feeling from my chest down. I could barely cut my food," Molson remembers. Molson was diagnosed with MS when she was 21, and within five years she needed full-time care. "It was scary. [The procedure] was my last shot at living." MS is among the most common chronic inflammatory diseases of the central nervous system, affecting an estimated two million people worldwide. New Canadian research led by two Ottawa doctors and published in The Lancet medical journal on Thursday suggests the high-risk therapy may stop the disease from progressing. "This is the first treatment to produce this level of disease control or neurological recovery" from MS, said The Lancet in a news release. But The Lancet also highlights the high mortality rate associated with the procedure — one patient out of 24 involved in the clinical trial died from liver failure. "Treatment related risks limit [the therapy's] widespread use," The Lancet concludes. Results 'impressive' Nevertheless, in the journal's accompanying editorial a German doctor calls the results "impressive." ©2016 CBC/Radio-Canada.
By JAMES GORMAN This summer’s science horror blockbuster is a remake: Return of the Leaping Electric Eel! If you have any kind of phobia of slimy, snakelike creatures that can rise from the water and use their bodies like Tasers, this story — and the accompanying video — may not be for you. The original tale (there was, alas, no video) dates to 1800 when the great explorer Alexander von Humboldt was in South America and enlisted local fishermen to catch some of these eels for the new (at the time) study of electricity. He wrote that the men herded horses and mules into a shallow pond and let the eels attack by pressing themselves against the horses. The horses and mules tried to escape, but the fishermen kept them in the water until the eels used up their power. Two horses died, probably from falling and drowning. Or so Humboldt said. Though the story was widely retold, no other report of this kind of fishing-with-horses phenomenon surfaced for more than 200 years, according to Kenneth Catania, a scientist with a passion for studying the eel species in question, electrophorus electricus. In 2014, he reported on how the eels freeze their prey. They use rapid pulses of more than 600 volts generated by modified muscle cells and sent through the water. These volleys of shocks cause the muscles of prey to tense at once, stopping all movement. The eels’ bodies function like Tasers, Dr. Catania wrote. But they can also project high-voltage pulses in the water in isolated couplets rather than full volleys for a different effect. The pairs of shocks don’t freeze the prey, but cause their bodies to twitch. That movement reveals the prey’s location, and then the eels send out a rapid volley to immobilize then swallow it. Dr. Catania noticed another kind of behavior, however. He was using a metal-handled net — wearing rubber gloves — while working with eels in an aquarium, and the eels would fling themselves up the handle of the net, pressing themselves to the metal and generating rapid electric shocks. © 2016 The New York Times Company
James Gorman Fruit flies are far from human, but not as far as you might think. They do many of the same things people do, like seek food, fight and woo mates. And their brains, although tiny and not set up like those of humans or other mammals, do many of the same things that all brains do — make and use memories, integrate information from the senses, and allow the creature to navigate both the physical and the social world. Consequently, scientists who study how all brains work like to use flies because it’s easier for them to do invasive research that isn’t allowed on humans. The technology of neuroscience is sophisticated enough to genetically engineer fly brains, and to then use fluorescent chemicals to indicate which neurons are active. But there are some remaining problems, like how to watch the brain of a fly that is moving around freely. It is one thing to record what is going on in a fly’s brain if the insect’s movement is restricted, but quite another to try to catch the light flash of brain cells from a fly that is walking around. Takeo Katsuki, an assistant project scientist at the Kavli Institute at the University of California, San Diego, is interested in courtship. And, he said, fruit flies simply won’t engage in courtship when they are tethered. So he and Dhruv Grover, another assistant project scientist, and Ralph J. Greenspan, in whose lab they both work, set out to develop a method for recording the brain activity of a walking fly. One challenge was to track the fly as it moved. They solved that problem with three cameras to follow the fly and a laser to activate the fluorescent chemicals in the brain. © 2016 The New York Times Company
Scientists say they have found a gene that causes a rare but inherited form of multiple sclerosis. It affects about one in every thousand MS patients and, according to the Canadian researchers, is proof that the disease is passed down generations. Experts have long suspected there's a genetic element to MS, but had thought there would be lots of genes involved, as well as environmental factors. The finding offers hope of targeted screening and therapy, Neuron reports. The University of British Columbia studied the DNA of hundreds of families affected by MS to hunt for a culprit gene. They found it in two sets of families containing several members with a rapidly progressive type of MS. In these families, 70% of the people with the mutation developed the disease. Although other factors may still be important and necessary to trigger the disease process, the gene itself is a substantial causative risk factor that is passed down from parents to their children, say the researchers. The mutation is in a gene called NR1H3, which makes a protein that acts as a switch controlling inflammation. In MS the body's immune system mistakenly attacks the protective layer of myelin that surrounds nerve fibres in the brain and spinal cord, leading to muscle weakness and other symptoms. Studies in mice show that knocking out the function of the same gene leads to neurological problems and decreased myelin production. © 2016 BBC.