Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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By Esther Hsieh Imagine you are enjoying your golden years, driving to your daily appointment for some painless brain zapping that is helping to stave off memory loss. That's the hope of a new study, in which people who learned associations (such as a random word and an image) after transcranial magnetic stimulation (TMS) were better able to learn more pairings days and weeks later—with no further stimulation needed. TMS uses a magnetic coil placed on the head to increase electrical signaling a few centimeters into the brain. Past studies have found that TMS can boost cognition and memory during stimulation, but this is the first to show that such gains can last even after the TMS regimen is completed. In the new study, which was published in Science, neuroscientists first used brain imaging to identify the associative memory network of 16 young, healthy participants. This network, based around the hippocampus, glues together things such as sights, places, sounds and time to form a memory, explains neuroscientist Joel Voss of Northwestern University, a senior author of the paper. Next, the researchers applied TMS behind the left ear of each participant for 20 minutes for five consecutive days to stimulate this memory network. To see if participants' associative memory improved, one day after the stimulation regimen finished they were tested for their ability to learn random words paired with faces. Subjects who had had TMS performed 33 percent better, compared with those who received placebo treatments, such as sham stimulation. © 2015 Scientific American
Richard Harris American medicine is heading into new terrain, a place where a year's supply of drugs can come with a price tag that exceeds what an average family earns. Pharmacy benefit manager Express Scripts says last year more than half a million Americans racked up prescription drug bills exceeding $50,000. Barbara Haedtke of Portland, Ore., knows this all too well. When she was diagnosed with multiple sclerosis in 2001 at the age of 35, she was prescribed Avonex, at a cost of around $10,000 a year. Her health insurance paid most of that until she and her husband found themselves without jobs during an economic downturn. "We were in the hole, and so $10,000 was a lot of money," she says. "Under the best circumstances it's a lot of money, but then particularly it was really difficult." Barbara Haedtke says she's grateful for a drug-company program that helps cover copays, but doesn't know how long she'll get that benefit. The drug company gave her the medication at no charge until she once again had a job with insurance, and for that, she says, she's really grateful. But the story doesn't end there. Haedtke used Avonex for about a decade and watched with disbelief as the price more than tripled. She's now taking a new drug, Tecfidera, that's priced even higher — $66,000 a year, according to her pharmacy receipt. The drug is supposed to help reduce the number of episodes that characterize multiple sclerosis, a disease in which nerve fibers gradually degenerate, causing muscle weakness, numbness, loss of balance and even paralysis. © 2015 NPR
Nick Davis Mood disorders such as depression are devastating to sufferers, and hugely costly to treat. The most severe form of depression, often called clinical depression or major depressive disorder (MDD), increases the person’s likelihood of suicide and contributes significantly to a person’s disability-adjusted life years (DALYs), a measure of quality of life taking into account periods of incapacity. The healthcare burden of MDD is large in most countries, especially when the person requires a stay in hospital. Putting these factors together, it’s clear we need to develop effective treatments to combat depression. The mechanisms of depressive disorders are not well understood, and it seems likely that there is no single cause. Most modern therapies use drugs that target neurotransmitters – the chemicals that carry signals between neurons. For example, the class of drugs known as SSRIs, or selective serotonin reuptake inhibitors, prevent the neurotransmitter serotonin from being reabsorbed by a neuron; this means that more serotonin is available to wash around between the nerve cells, and is more likely to activate cells in the brain networks that area affected in MDD. But SSRIs and other drugs are not a pharmacological ‘free lunch’. Drug treatments for depression are ineffective for many people, cause side-effects, and may lose their therapeutic effect over time. For these reasons, many researchers are searching for alternative treatments for MDD that overcome these problems, and are more effective or less unpleasant. One potential treatment involves the use of pulses of magnetic energy over the head to target the brain’s mood circuits. This technique, called transcranial magnetic stimulation (TMS), may potentially address some of the problems of pharmaceutical treatments, but we still don’t know exactly how it works, or how effective it will be in treating MDD. © 2015 Guardian News and Media Limited
Link ID: 20946 - Posted: 05.18.2015
Backyard Brains. For 235 years we have been trying to isolate, understand, and analyze the elusive action potential, and here we tell the story that continues today. The progress of understanding Action Potentials can be classed into three main endeavors: 1. Amplification The amplifiers that gave us the first hint of the electrical impulses generated by neurons came from biological tissue itself! Scientists of the 18th and early 19th century used the contractions of muscles as "bioamplifiers" to indirectly measure neural firing. Using friction machines (spark generators), Leyden jars (primitive capacitors), or Voltaic Piles (the first batteries), electrical stimuli could be delivered to motor neurons that were still attached to muscles. The electrical stimulation would cause the nerve to fire action potentials (so people hypothesized), the muscle would then contract, and the force of contraction could be measured with a spring. With increasing electrical stimuli strength (thus more action potentials in the motor neurons), the muscle would contract with increasing force. This technique worked, but led to vigorous debates as to whether the neural tissue was actually generating its own action potentials at all, or whether the muscle contraction was just a direct result of electrical stimulation. By the mid-19th century, galvanometers had been invented, and it was possible to see that nerves were indeed generating their own action potentials. These galvanometers exploited the then new technology of electromagnets. For example, Emil de Bois-Reymond built by hand a type of galvanometer with 24,000 turns around an iron plate. When the nerve fired action potentials, a metal needle suspended by the plate would deflect. These devices worked, but the needle movement was not fast enough to separate the 1 ms individual action potentials, and the machines occupied a lot of time to construct. © 2009-2015 Backyard Brains
Link ID: 20944 - Posted: 05.18.2015
By GREGORY HICKOK IN 1890, the American psychologist William James famously likened our conscious experience to the flow of a stream. “A ‘river’ or a ‘stream’ are the metaphors by which it is most naturally described,” he wrote. “In talking of it hereafter, let’s call it the stream of thought, consciousness, or subjective life.” While there is no disputing the aptness of this metaphor in capturing our subjective experience of the world, recent research has shown that the “stream” of consciousness is, in fact, an illusion. We actually perceive the world in rhythmic pulses rather than as a continuous flow. Some of the first hints of this new understanding came as early as the 1920s, when physiologists discovered brain waves: rhythmic electrical currents measurable on the surface of the scalp by means of electroencephalography. Subsequent research cataloged a spectrum of such rhythms (alpha waves, delta waves and so on) that correlated with various mental states, such as calm alertness and deep sleep. Researchers also found that the properties of these rhythms varied with perceptual or cognitive events. The phase and amplitude of your brain waves, for example, might change if you saw or heard something, or if you increased your concentration on something, or if you shifted your attention. But those early discoveries themselves did not change scientific thinking about the stream-like nature of conscious perception. Instead, brain waves were largely viewed as a tool for indexing mental experience, much like the waves that a ship generates in the water can be used to index the ship’s size and motion (e.g., the bigger the waves, the bigger the ship). Recently, however, scientists have flipped this thinking on its head. We are exploring the possibility that brain rhythms are not merely a reflection of mental activity but a cause of it, helping shape perception, movement, memory and even consciousness itself. What this means is that the brain samples the world in rhythmic pulses, perhaps even discrete time chunks, much like the individual frames of a movie. From the brain’s perspective, experience is not continuous but quantized. © 2015 The New York Times Company
By Kira Peikoff I draw an uneasy breath as I step into a bright purple office on the 14th floor of Boston’s Prudential Building. I am shown to a small conference table, where I take a seat and await the experiment. A palm-size triangular module is affixed above my right eye. It connects to a single-use strip of electrodes stuck onto my forehead and running down the back of my neck. This is Thync, the latest in transcranial direct current stimulation, or tDCS. The manufacturer says the device, to come out later this year, can alter the user’s mood in minutes via electric current. With a connected smartphone app, the mood-impaired subject chooses one of two settings: “calm vibes” or “energy vibes.” I tap “calm vibes” and wait. Somehow, I am having a hard time picturing myself unwinding at home this way while my husband sips a glass of Merlot. Thync is the latest in a wave of wearable gadgets offering so-called noninvasive brain stimulation. Until recently, it was mostly hobbyists — nine-volt batteries stuck to their heads — who experimented with tDCS as a means of improving concentration, verbal and computation abilities, and creativity. But in the last few years, several companies have introduced slick consumer devices, among them Foc.us, whose headset and controller cost $298, and The Brain Stimulator, whose advanced starter kit costs $150. In January, the journal Brain Stimulation published the largest meta-analysis of tDCS to date. After examining every finding replicated by at least two research groups, leading to 59 analyses, the authors reported that one session of tDCS failed to show any significant benefit for users. © 2015 The New York Times Company
Link ID: 20891 - Posted: 05.05.2015
By Ashley Yeager The image is made using Brainbow, a technique developed in 2007 that inserts genes for fluorescent proteins into animals. When activated, the proteins illuminate some cells in a range of colors. While most researchers use Brainbow to visualize connections between nerve cells in the brain, Alain Chédotal of the Institut de la Vision in Paris and colleagues customized the technique to trace networks of cells called oligodendrocytes. These cells wrap a material called myelin, the biological equivalent of electrical insulation, around long strands of nerve cells that transmit electrical signals in the brain and throughout the body. How oligodendrocytes work together to wrap nerve fibers in myelin becomes evident in Brainbow photos of the roughly 3-millimeter-long optic nerve, the team reports in the April Glia. The myelin shields the precious link between brain and eyes. Studying interactions among oligodendrocytes as well as the cells’ reactions to various drugs may lead to improved therapies for multiple sclerosis, a disease caused by the destruction of myelin. Citations L. Dumas et al. Multicolor analysis of oligodendrocyte morphology, interactions, and development with Brainbow. Glia. Vol. 63, April 2015, p. 699. doi: 10.1002/glia.22779 © Society for Science & the Public 2000 - 2015.
By REUTERS NEW YORK — The mouse walked, the mouse stopped; the mouse ignored a bowl of food, then scampered back and gobbled it up, and it was all controlled by neuroscientists, researchers reported on Thursday. The study, describing a way to manipulate a lab animal's brain circuitry accurately enough to turn behaviors both on and off, is the first to be published under President Barack Obama's 2013 BRAIN Initiative, which aims to advance neuroscience and develop therapies for brain disorders. The point of the remote-control mouse is not to create an army of robo-rodents. Instead, neuroscientists hope to perfect a technique for identifying brain wiring underlying any behavior, and control that behavior by activating and deactivating neurons. If scientists are able do that for the circuitry involved in psychiatric or neurological disorders, it may lead to therapies. That approach reflects a shift away from linking such illnesses to "chemical imbalances" in the brain, instead tracing them to miswiring and misfiring in neuronal circuits. "This tool sharpens the cutting edge of research aimed at improving our understanding of brain circuit disorders, such as schizophrenia and addictive behaviors," said Dr. Francis Collins, director of the National Institutes of Health, which funded the $1 million study. The technique used to control neurons is called DREADDs (designer receptors exclusively activated by designer drugs). Brain neurons are genetically engineered to produce a custom-made - "designer" - receptor. When the receptor gathers in a manmade molecule that fits like a key in a lock, the neuron is activated. © 2015 The New York Times Company
Keyword: Brain imaging
Link ID: 20881 - Posted: 05.04.2015
By Emily DeMarco Mice and rats communicate in the ultrasonic frequency range, and it’s thought that cats evolved the ability to hear those high-pitched squeaks to better hunt their prey. Now, a new study suggests that sensitivity to higher pitched sounds may cause seizures in some older cats. After receiving reports of the problem, nicknamed the “Tom and Jerry syndrome” because of how the cartoon cat is often startled by sounds, researchers surveyed cat owners and examined their pets’ medical records, looking for insight into the types and durations of seizures and the sounds that provoked them. In 96 cats, they found evidence of the syndrome they call feline audiogenic reflex seizures. The most common types of seizure-eliciting sounds included crinkling tinfoil, clanking a metal spoon on a ceramic feeding bowl, and clinking glass. The severity of the seizure ranged from brief muscle jerks to more serious episodes where the cat lost consciousness and stiffened and jerked for several minutes, the researchers report online today in the Journal of Feline Medicine and Surgery. Both pedigree and nonpedigree cats were susceptible, although one breed was common: Thirty of the 96 cats were Birmans (pictured). Because the seizures coincided with old age—the average age of onset was 15 years—veterinarians could miss the disorder while dealing with the felines’ other health issues, the researchers say. Minimizing exposure to the problematic sounds and preliminary, therapeutic trials with levetiracetam—an anticonvulsant medication used to control epilepsy—among a small sample of the cats seemed to help limit the occurrence of seizures. © 2015 American Association for the Advancement of Science.
Jon Hamilton The simple act of thinking can accelerate the growth of many brain tumors. That's the conclusion of a paper in Cell published Thursday that showed how activity in the cerebral cortex affected high-grade gliomas, which represent about 80 percent of all malignant brain tumors in people. "This tumor is utilizing the core function of the brain, thinking, to promote its own growth," says Michelle Monje, a researcher and neurologist at Stanford who is the paper's senior author. In theory, doctors could slow the growth of these tumors by using sedatives or other drugs to reduce mental activity, Monje says. But that's not a viable option because it wouldn't eliminate the tumor and "we don't want to stop people with brain tumors from thinking or learning or being active." Even so, the discovery suggests other ways to slow down some of the most difficult brain tumors, says Tracy Batchelor, who directs the neuro-oncology program at Massachusetts General Hospital and was not involved in the research. "We really don't have any curative treatments for high-grade gliomas," Batchelor says. The discovery of a link between tumor growth and brain activity "has opened up a window into potential therapeutic interventions," he says. The discovery came from a team of scientists who studied human glioma tumors implanted in mouse brains. The scientists used a technique called optogenetics, which uses light to control brain cells, to increase the activity of cells near the tumors. © 2015 NPR
Link ID: 20846 - Posted: 04.25.2015
By Antonio Regalado Various powerful new tools for exploring and manipulating the brain have been developed over the last few years. Some use electronics, while others use light or chemicals. At one MIT lab, materials scientist Polina Anikeeva has hit on a way to manufacture what amounts to a brain-science Swiss Army knife. The neural probes she builds carry light while collecting and transmitting electricity, and they also have tiny channels through which to pump drugs. That’s an advance over metal wires or silicon electrodes conventionally used to study neurons. Anikeeva makes the probes by assembling polymers and metals into large-scale blocks, or preforms, and then stretching them into flexible, ultrathin fibers. Multifunctional fibers offer new ways to study animal behavior, since they can record from neurons as well as stimulating them. New types of medical technology could also result. Imagine, as Anikeeva does, bionic wiring that bridges a spinal-cord injury, collecting electrical signals from the brain and transmitting them to the muscles of a paralyzed hand. Anikeeva made her first multifunctional probe while studying at Stanford. It was crude: she simply wrapped metal wires around a glass filament. But this made it possible to combine standard electrode measurements with a new technology, optogenetics, in which light is fired at neurons to activate them or shut them down.
Keyword: Brain imaging
Link ID: 20832 - Posted: 04.22.2015
Heidi Ledford An experimental antibody drug aimed at protecting nerves from the ravages of multiple sclerosis offers hope for a new way to combat the neurological disease — if researchers can definitively show that it works. The antibody, anti-LINGO-1, is intended to stimulate regrowth of the myelin sheath, the fatty protective covering on nerve cells that is damaged by multiple sclerosis. Its developer, Biogen of Cambridge, Massachusetts, will present results from a small clinical trial at an American Academy of Neurology meeting this week in Washington DC. If the initial promising results from the trial are confirmed, it will be the first such myelin-regeneration therapy. Other researchers are racing to find more targets and compounds that act similarly. “Once we get a positive result, the field will move very quickly,” says Jack Antel, a neurologist at McGill University in Montreal, Canada. But that excitement is tempered by practical hurdles: there is as yet no proven way to measure remyelination of nerve cells in living humans. Myelin sheaths insulate and support axons, the fibres that transmit signals between nerve cells. In multiple sclerosis, immune attack destroys these sheaths. Stripped of this protective coating, the axons gradually wither away, causing the numbness and muscle spasms that are characteristic of the disease. The 12 drugs approved in the United States to treat multiple sclerosis slow this immune attack — although sometimes with dangerous side effects. But none stops it, says Bruce Trapp, a neuroscientist at the Cleveland Clinic in Ohio. © 2015 Nature Publishing Group
Two drugs already on the market — an antifungal and a steroid — may potentially take on new roles as treatments for multiple sclerosis. According to a study published in Nature today, researchers discovered that these drugs may activate stem cells in the brain to stimulate myelin producing cells and repair white matter, which is damaged in multiple sclerosis. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. Specialized cells called oligodendrocytes lay down multiple layers of a fatty white substance known as myelin around axons, the long “wires” that connect brain cells. Myelin acts as an insulator and enables fast communication between brain cells. In multiple sclerosis there is breakdown of myelin and this deterioration leads to muscle weakness, numbness and problems with vision, coordination and balance. “To replace damaged cells, the scientific field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road. We asked if we could find a faster and less invasive approach by using drugs to activate native nervous system stem cells and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself,” said Paul J. Tesar, Ph.D., associate professor at Case Western Reserve School of Medicine in Cleveland, and senior author of the study. It is unknown how myelin-producing cells are damaged, but research suggests they may be targeted by malfunctioning immune cells and that multiple sclerosis may start as an autoimmune disorder. Current therapies for multiple sclerosis include anti-inflammatory drugs, which help prevent the episodic relapses common in multiple sclerosis, but are less effective at preventing long-term disability. Scientists believe that therapies that promote myelin repair might improve neurologic disability in people with multiple sclerosis.
Carl Zimmer In 1998, Dr. Philip A. Starr started putting electrodes in people’s brains. A neurosurgeon at the University of California, San Francisco, Dr. Starr was treating people with Parkinson’s disease, which slowly destroys essential bits of brain tissue, robbing people of control of their bodies. At first, drugs had given his patients some relief, but now they needed more help. After the surgery, Dr. Starr closed up his patients’ skulls and switched on the electrodes, releasing a steady buzz of electric pulses in their brains. For many patients, the effect was immediate. “We have people who, when they’re not taking their meds, can be frozen,” said Dr. Starr. “When we turn on the stimulator, they start walking.” First developed in the early 1990s, deep brain stimulation, or D.B.S., was approved by the Food and Drug Administration for treating Parkinson’s disease in 2002. Since its invention, about 100,000 people have received implants. While D.B.S. doesn’t halt Parkinson’s, it can turn back the clock a few years for many patients. Yet despite its clear effectiveness, scientists like Dr. Starr have struggled to understand what D.B.S. actually does to the brain. “We do D.B.S. because it works,” said Dr. Starr, “but we don’t really know how.” In a recent experiment, Dr. Starr and his colleagues believe they found a clue. D.B.S. may counter Parkinson’s disease by liberating the brain from a devastating electrical lock-step. The new research, published on Monday in Nature Neuroscience, may help scientists develop better treatments for Parkinson’s disease. It may also help researchers adapt D.B.S. for treatment of such brain disorders as depression and obsessive compulsive disorder. © 2015 The New York Times Company
Link ID: 20817 - Posted: 04.18.2015
By Lenny Bernstein Children with two of the most severe forms of epilepsy can suffer scores of seizures each day, as well as long-term physical and cognitive problems. The two conditions, Dravet and Lennox-Gastaut syndromes, are quite rare but unfortunately very resistant to treatment with current epilepsy drugs. Now a compound found in marijuana plants has shown promising results in a preliminary study, during which it sharply reduced the number of seizures suffered by these children. Some were even seizure-free after three months of taking the drug, cannabidiol, the research showed. "We're very encouraged by the data," said Orrin Devinsky, director of the NYU Langone Comprehensive Epilepsy Center and leader of the research. A more rigorous study of cannabidiol's impact has begun and will help determine how effective it really is, he said. In making cannabidiol, the marijuana plant's psychoactive material (THC) was removed. A 99 percent pure liquid version of the drug was given for three to six months to 137 people with the two syndromes. Most were children (the subjects ranged in age from 2 to 26), and before the experiment they suffered a disturbing average of 95.3 convulsive seizures every month. Convulsive seizures are the more severe, violent kind; people with epilepsy can experience a wide variety of seizures, including some mild enough that they appear to be merely staring into space for a few seconds. Some of the subjects had taken as many as 10 different epilepsy drugs, with little success.
By Jennifer Couzin-Frankel Sudden death, a mysterious and devastating outcome of epilepsy, could result from a brain stem shutdown following a seizure, researchers report today in Science Translational Medicine. Although the idea is still preliminary, it’s engendering hope that neurologists are one step closer to intervening before death strikes. Sudden unexpected death in epilepsy (SUDEP) has long bedeviled doctors and left heartbroken families in its wake. “It’s as big a mystery as epilepsy itself,” says Jeffrey Noebels, a neurologist at Baylor College of Medicine in Houston, Texas, and the senior author of the new paper. As its name suggests, SUDEP attacks without warning: People with epilepsy are found dead, often following a seizure, sometimes face down in bed. Many are young—the median age is 20—and patients with uncontrolled generalized seizures, the most severe type, are at highest risk. About 3000 people are thought to die of SUDEP each year in the United States. And doctors have struggled to understand why. “How can you have seizures your whole life, and all of a sudden, it’s your last one?” Noebels asks. In 2013, an international team of researchers described its study of epilepsy patients who had died while on hospital monitoring units. In 10 SUDEP cases for which they had the patients’ heart function and breathing patterns, the authors found that the patients’ cardiorespiratory systems collapsed over several minutes, and their brain activity was severely depressed. “Their EEG went flat after a seizure,” says Stephan Schuele, an epileptologist at Northwestern University Feinberg School of Medicine in Chicago, Illinois, who wasn’t involved in the study. © 2015 American Association for the Advancement of Science
Link ID: 20782 - Posted: 04.10.2015
|By Simon Makin People can control prosthetic limbs, computer programs and even remote-controlled helicopters with their mind, all by using brain-computer interfaces. What if we could harness this technology to control things happening inside our own body? A team of bioengineers in Switzerland has taken the first step toward this cyborglike setup by combining a brain-computer interface with a synthetic biological implant, allowing a genetic switch to be operated by brain activity. It is the world's first brain-gene interface. The group started with a typical brain-computer interface, an electrode cap that can register subjects' brain activity and transmit signals to another electronic device. In this case, the device is an electromagnetic field generator; different types of brain activity cause the field to vary in strength. The next step, however, is totally new—the experimenters used the electromagnetic field to trigger protein production within human cells in an implant in mice. The implant uses a cutting-edge technology known as optogenetics. The researchers inserted bacterial genes into human kidney cells, causing them to produce light-sensitive proteins. Then they bioengineered the cells so that stimulating them with light triggers a string of molecular reactions that ultimately produces a protein called secreted alkaline phosphatase (SEAP), which is easily detectable. They then placed the human cells plus an LED light into small plastic pouches and inserted them under the skin of several mice. © 2015 Scientific American
Hannah Devlin, science correspondent Scientists have raised the alert about an antibiotic routinely prescribed for chest infections, after linking it to an increased risk of epilepsy and cerebral palsy in children whose mothers took the drug during pregnancy. Children of mothers who had taken macrolide antibiotics were found to be almost twice as likely to be affected by the conditions, prompting scientists to call for a review of their use during pregnancy. The study authors urged pregnant women not to stop taking prescribed antibiotics, however. The potential adverse effects are rare and, as yet, unproven, while infections during pregnancy are a well-established cause of health problems in babies. Professor Ruth Gilbert, a clinical epidemiologist who led the research at University College London, said: “The main message is for medicines regulators and whether they need to issue a warning about these drugs. For women, if you’ve got a bacterial infection, it’s more important to get on and treat it.” The study tracked the children of nearly 65,000 women who had been prescribed a variety of antibiotics for illnesses during pregnancy, including chest and throat infections and cystitis. There was no evidence that most antibiotics (including penicillin, which made up 67% of prescriptions), led to an increased risk of the baby developing cerebral palsy or epilepsy. However, when the antibiotics were compared head-to-head, the potential adverse effect of macrolide drugs emerged. Around 10 in 1,000 children whose mothers were given the drug had developed the conditions by the age of seven, compared to 6 in 1,000 children, for those who had other types of antibiotic. © 2015 Guardian News and Media Limited
Mo Costandi Two teams of scientists have developed new ways of stimulating neurons with nanoparticles, allowing them to activate brain cells remotely using light or magnetic fields. The new methods are quicker and far less invasive than other hi-tech methods available, so could be more suitable for potential new treatments for human diseases. Researchers have various methods for manipulating brain cell activity, arguably the most powerful being optogenetics, which enables them to switch specific brain cells on or off with unprecedented precision, and simultaneously record their behaviour, using pulses of light. This is very useful for probing neural circuits and behaviour, but involves first creating genetically engineered mice with light-sensitive neurons, and then inserting the optical fibres that deliver light into the brain, so there are major technical and ethical barriers to its use in humans. Nanomedicine could get around this. Francisco Bezanilla of the University of Chicago and his colleagues knew that gold nanoparticles can absorb light and convert it into heat, and several years ago they discovered that infrared light can make neurons fire nervous impulses by heating up their cell membranes. They therefore attached gold nanorods to three different molecules that recognise and bind to proteins in the cell membranes – the scorpion toxin Ts1, which binds to a sodium channel involved in producing nervous impulses, and antibodies that bind the P2X3 and the TRPV1 channels, both found in dorsal root ganglion (DRG) neurons, which transmit touch and pain information up the spinal cord and into the brain. © 2015 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 20717 - Posted: 03.25.2015
By Emily Underwood Deep brain stimulation, which now involves surgically inserting electrodes several inches into a person's brain and connecting them to a power source outside the skull, can be an extremely effective treatment for disorders such as Parkinson's disease, obsessive compulsive disorder, and depression. The expensive, invasive procedure doesn't always work, however, and can be risky. Now, a study in mice points to a less invasive way to massage neuronal activity, by injecting metal nanoparticles into the brain and controlling them with magnetic fields. Major technical challenges must be overcome before the approach can be tested in humans, but the technique could eventually provide a wireless, nonsurgical alternative to traditional deep brain stimulation surgery, researchers say. "The approach is very innovative and clever," says Antonio Sastre, a program director in the Division of Applied Science & Technology at the National Institute of Biomedical Imaging and Bioengineering in Bethesda, Maryland. The new work provides "a proof of principle." The inspiration to use magnets to control brain activity in mice first struck materials scientist Polina Anikeeva while working in the lab of neuroscientist-engineer Karl Deisseroth at Stanford University in Palo Alto, California. At the time, Deisseroth and colleagues were refining optogenetics, a tool that can switch specific ensembles of neurons on and off in animals with beams of light. © 2015 American Association for the Advancement of Science.
Keyword: Brain imaging
Link ID: 20690 - Posted: 03.14.2015