Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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By Julianne Chiaet It has taken a century so far for scientists to not figure out the cause of multiple sclerosis (MS). The inflammatory disease, which affects more than 2.1 million people worldwide, has been blamed on toxins, viruses and even food. Most recently, scientists have placed their bets on two major ideas: The first (and far more popular) hypothesis suggests MS begins in white matter, which influences how parts of the brain work together. White matter consists of bundles of axons covered in myelin, a white insulating fatty layer. In people with MS myelin degrades and nerve fibers are left exposed, causing problems in motor coordination and loss of senses. The second hypothesis suggests that MS begins in the gray matter, which affects thinking and learning. The white matter hypothesis overshadows its alternative in part because white matter’s impact is easier to observe. When using a microscope to look at brain tissue, scientists are struck by the degradation in the myelin in samples from patients with MS. And when analyzing MS in the clinic, the overt symptoms experienced by a person with the disease can be attributed to the myelin. Symptoms associated with dysfunctions in gray matter are less obvious, such as the loss of an IQ point. Now, new evidence lends support to the less-favored gray matter hypothesis. Scientists at Rutgers University in Newark tried a new approach to look into the gray matter of MS patients. They analyzed proteins in cerebrospinal fluid (CSF), which can be thought of as the central nervous system’s “blood.” By comparing the quantity of specific CSF proteins in patients who were newly diagnosed or had the relapsing remitting variety of MS with that of healthy patients, the researchers found an uneven distribution of 20 proteins among the three groups. © 2013 Scientific American
by Andy Coghlan Parts of the brain may still be alive after a person's brain activity is said to have flatlined. When someone is in a deep coma, their brain activity can go silent. An electroencephalogram measuring this activity may eventually show a flatline, usually taken as a sign of brain death. However, while monitoring a patient who had been placed in a deep coma to prevent seizures following a cardiac arrest, Bogdan Florea, a physician at the Regina Maria Medical Centre in Cluj-Napoca, Romania, noticed a strange thing – some tiny intermittent bursts of activity were interrupting an otherwise flatline signal, each lasting a few seconds. He asked Florin Amzica of the University of Montreal in Canada and his colleagues to investigate what might be happening. To imitate what happened in the patient, Amzica's team put cats into a deep coma using a high dose of anaesthesia. While EEG recordings taken from the surface of the brain – the cortex – showed a flatline, recordings from deep-brain electrodes revealed tiny bursts of activity originating in the hippocampus, responsible for memory and learning, which spread within minutes to the cortex. "These ripples build up a synchrony that rises in a crescendo to reach a threshold where they can spread beyond the hippocampus and trigger activity in the cortex," says Amzica. © Copyright Reed Business Information Ltd.
Link ID: 18683 - Posted: 09.21.2013
By Associated Press, Former Grateful Dead drummer Mickey Hart has a new piece of equipment accompanying him on his latest tour: a cap fitted with electrodes that capture his brain activity and direct the movements of a light show while he’s jamming on stage. The sensor-studded headgear is an outgrowth of collaboration between Hart, 70, and Adam Gazzaley, a University of California at San Francisco neuroscientist who studies cognitive decline. The subject has been an interest of the musician’s since the late 1980s, as he watched his grandmother deal with Alzheimer’s disease. When he played the drums for her, he says, she became more responsive. Since then, Hart has invested time and money exploring the therapeutic potential of rhythm. Thirteen years ago, he founded Rhythm for Life, a nonprofit promoting drum circles for the elderly. Hart first publicly wore his electroencephalogram cap last year at an AARP convention where he and Gazzaley discussed their joint pursuit of research on the link between brain waves and memory. He wore it again while making his new album, “Superorganism,” translating the rhythms of his brain waves into music. Hart’s bandmates, with input from other researchers in Gazzaley’s lab, paired different waves with specific musical sequences that were then inserted into songs. © 1996-2013 The Washington Post
Two pioneers in the study of neural signaling and three researchers responsible for modern cochlear implants are winners of The Albert and Mary Lasker Foundation’s annual prize, announced today. The prestigious award honoring contributions in the medical sciences is often seen as a hint at future Nobel contenders. The prizes for basic and clinical research each carry a $250,000 honorarium. Richard Scheller of the biotech company Genentech and Thomas Südhof of Stanford University in Palo Alto, California, got their basic research Laskers for discovering the mechanisms behind rapid the release of neurotransmitters—the brain’s chemical messengers—into the space between neurons. This process underlies all communication among brain cells, and yet it was “a black box” before Scheller and Südhof’s work, says their colleague Robert Malenka, a synaptic physiologist at Stanford. The two worked independently in the late 1980s to identify individual proteins that mediate the process, and their development of genetically altered mice lacking these proteins was “an ambitious and high-risk approach,” Malenka says. Although “they weren’t setting out to understand any sort of disease,” their discoveries have helped unravel the genetic basis for neurological disorders such as Parkinson’s disease. This year’s clinical research prizes went to Graeme Clark, Ingeborg Hochmair, and Blake Wilson for their work to restore hearing to the deaf. In the 1970s, Hochmair and Clark of the cochlear implant company MED-EL in Innsbruck, Austria, and the University of Melbourne, respectively, were the first to insert multiple electrodes into the human cochlea to stimulate nerves that respond to different frequencies of sound. © 2012 American Association for the Advancement of Science
By Athena Andreadis Recently, two studies surfaced almost simultaneously that led to exclamations of “Vulcan mind meld!”, “Zombie armies!” and “Brains in jars!” One is the announcement by Rajesh Rao and Andrea Stocco of Washington U. that they “achieved the first human-to-human brain interface”. The other is the Nature paper by Madeline Lancaster et al about stem-cell-derived “organoids” that mimic early developmental aspects of the human cortex. My condensed evaluation: the latter is far more interesting and promising than the former, which doesn’t quite do what people (want to) think it’s doing. The purported result of brain interfacing hit many hot buttons that have been staples of science fiction and Stephen King novels: primarily telepathy, with its fictional potential for non-consensual control. Essentially, the sender’s EEG (electroencephalogram) output was linked to the receiver’s TMS (transcranial magnetic stimulation) input. What the experiment actually did is not send a thought but induce a muscle twitch; nothing novel, given the known properties of the two technologies. The conditions were severely constrained to produce the desired result and I suspect the outcome was independent of the stimulus details: the EEG simply recorded that a signal had been produced and the TMS apparatus was positioned so that a signal would elicit a movement of the right hand. Since both sender and receiver were poised over a keyboard operating a video game, the twitch was sufficient to press the space bar, programmed by the game to fire a cannon. © 2013 Scientific American
Link ID: 18623 - Posted: 09.10.2013
According to new research on epilepsy, zebrafish have certainly earned their stripes. Results of a study in Nature Communications suggest that zebrafish carrying a specific mutation may help researchers discover treatments for Dravet syndrome (DS), a severe form of pediatric epilepsy that results in drug-resistant seizures and developmental delays. Scott C. Baraban, Ph.D., and his colleagues at the University of California, San Francisco (UCSF), carefully assessed whether the mutated zebrafish could serve as a model for DS, and then developed a new screening method to quickly identify potential treatments for DS using these fish. This study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health and builds on pioneering epilepsy zebrafish models first described by the Baraban laboratory in 2005. Dravet syndrome is commonly caused by a mutation in the Scn1a gene, which encodes for Nav1.1, a specific sodium ion channel found in the brain. Sodium ion channels are critical for communication between brain cells and proper brain functioning. The researchers found that the zebrafish that were engineered to have the Scn1a mutation that causes DS in humans exhibited some of the same characteristics, such as spontaneous seizures, commonly seen in children with DS. Unprovoked seizure activity in the mutant fish resulted in hyperactivity and whole-body convulsions associated with very fast swimming. These types of behaviors are not seen in normal healthy zebrafish.
Link ID: 18603 - Posted: 09.04.2013
By Scicurious Optogenetics likes to light up debate. Optogenetics is a hot technique in neuroscience research right now, involving taking a light-activited gene (called a channel rhodopsin) targeted into a single neuron type, and inserting it into the genome of, say, a mouse (yes, we can do this now). When you then shine a light into the mouse’s brain, the channel rhodopsin responds, and the neurons that are now expressing the channel rhodopsin fire. This means that you can get a single type of neuron to fire (or not, there are ones that inhibit firing, too), whenever you want to, merely by turning on a light. I actually remember where I WAS when I first heard of optogenetics. I came into the lab in the morning, was going about my daily business, and hadn’t checked the daily Tables of Contents for journals yet (I get these delivered into my email). I remember the postdoc, normally a pretty phlegmatic person, actually putting a little excitement into their voice, “hey guys, look at this.” The paper was this one. We all crowded around. It took us all a few minutes to “get it”. As it began to sink it, I had two thoughts. The first? “WHOA, THAT IS AWESOME.” The second? “Great, I know what’s going to be the hot stuff now.” There are fashions in science. Not the kind where everyone dyes their lab coat plaid or creates cutoffs out of their Personal Protective Equipment (though that would be hilarious). There are experimental fashions. Lesions were once really “in”. Knockouts were hot stuff in the 90s. fMRI enjoyed (and still does enjoy) its moment in the sun, electrophysiology often adds a little je ne sais quoi to a paper. DREADDs, CLARITY. And when a new thing comes along and is going to be hot? You can sniff it out a mile away. For next year? I’m betting on GEVIs, myself. They’ll be all the rage. © 2013 Scientific American
Link ID: 18565 - Posted: 08.27.2013
By Scicurious There are lots of challenges when it comes to studying the brain, but one of the biggest is that it’s very hard to see. Aside from being, you know, inside your skull, the many electrical and chemical signals which the brain uses are impossible to see with the naked eye. We have ways to look at neurons and how they convey information. For example, to record the electrical signals from a single neuron, you can piece it with a tiny electrode, to get access inside the membrane (electrophysiology). You can then stimulate the neuron to fire, or record as it fires spontaneously. For techniques like optogenetics, you can insert a gene into the neuron that makes it fire (or not) in response to light. When you shine the light, you can make the neuron fire. So you can make a neuron fire, or see a neuron fire. With things like voltammetry, we can see neurotransmitters, chemicals as they are released from a neuron and sent as signals on to other neurons. Techniques like these have made huge strides in what we understand about neurons and how they work. But…you can only do this for a few neurons at a time. This becomes a problem, because the brain does not work as one neuron at a time. Instead, neurons organize into networks, A neuron fires, which impinges upon many more neurons, all of which will react in different ways, depending on what input they receive and when. Often many neurons have to fire to get a result, often it’s a single specific pattern of neurons. An ideal technique would be one where we could see neurons fire spontaneously, in real time, and then see where those signals GO, to actually see a network in action. And where we could see it…without taking the brain out first. It looks like that technique might be here. © 2013 Scientific American
Keyword: Brain imaging
Link ID: 18496 - Posted: 08.13.2013
Brain cells talk to each other in a variety of tones. Sometimes they speak loudly but other times struggle to be heard. For many years scientists have asked why and how brain cells change tones so frequently. Today National Institutes of Health researchers showed that brief bursts of chemical energy coming from rapidly moving power plants, called mitochondria, may tune brain cell communication. “We are very excited about the findings,” said Zu-Hang Sheng, Ph.D., a senior principal investigator and the chief of the Synaptic Functions Section at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “We may have answered a long-standing, fundamental question about how brain cells communicate with each other in a variety of voice tones.” The network of nerve cells throughout the body typically controls thoughts, movements and senses by sending thousands of neurotransmitters, or brain chemicals, at communication points made between the cells called synapses. Neurotransmitters are sent from tiny protrusions found on nerve cells, called presynaptic boutons. Boutons are aligned, like beads on a string, on long, thin structures called axons. They help control the strength of the signals sent by regulating the amount and manner that nerve cells release transmitters. Mitochondria are known as the cell’s power plant because they use oxygen to convert many of the chemicals cells use as food into adenosine triphosphate (ATP), the main energy that powers cells. This energy is essential for nerve cell survival and communication. Previous studies showed that mitochondria can rapidly move along axons, dancing from one bouton to another.
Link ID: 18414 - Posted: 07.27.2013
Silk has walked straight off the runway and into the lab. According to a new study published in the Journal of Clinical Investigation, silk implants placed in the brain of laboratory animals and designed to release a specific chemical, adenosine, may help stop the progression of epilepsy. The research was supported by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute of Biomedical Imaging and Bioengineering (NIBIB), which are part of the National Institutes of Health. The epilepsies are a group of neurological disorders associated with recurring seizures that tend to become more frequent and severe over time. Adenosine decreases neuronal excitability and helps stop seizures. Earlier studies have suggested abnormally low levels of adenosine may be linked to epilepsy. Rebecca L. Williams-Karnesky, Ph.D. and her colleagues from Legacy Research Institute, Portland, Ore., Oregon Health and Sciences University (OHSU), Portland, and Tufts University, Boston, looked at long-term effects of an adenosine-releasing silk-implant therapy in rats and examined the role of adenosine in causing epigenetic changes that may be associated with the development of epilepsy. The investigators argue that adenosine’s beneficial effects are due to epigenetic modifications (chemical reactions that change the way genes are turned on or off without altering the DNA code, the letters that make up our genetic background). Specifically, these changes happen when a molecule known as a methyl group blocks a portion of DNA, affecting which genes are accessible and can be turned on. If methyl groups have been taken away (demethylated), genes are more likely to turn on.
Link ID: 18409 - Posted: 07.27.2013
by Carl Zimmer Inside each of us is a miniature version of ourselves. The Canadian neurologist Wilder Penfield discovered this little person in the 1930s, when he opened up the skulls of his patients to perform brain surgery. He would sometimes apply a little electric jolt to different spots on the surface of the brain and ask his patients–still conscious–to tell him if they felt anything. Sometimes their tongues tingled. Other times their hand twitched. Penfield drew a map of these responses. He ended up with a surreal portrait of the human body stretched out across the surface of the brain. In a 1950 book, he offered a map of this so-called homunculus. For brain surgeons, Penfield’s map was a practical boon, helping them plan out their surgeries. But for scientists interested in more basic questions about the brain, it was downright fascinating. It revealed that the brain organized the sensory information coming from the skin into a body-like form. There were differences between the homunculus and the human body, of course. It was as if the face had been removed from the head and moved just out of reach. The area that each body part took up in the brain wasn’t proportional to its actual size. The lips and index finger were gigantic, for instance, while the forearm barely took up less space than the tongue. That difference in our brains is reflected in our nerve endings. Our fingertips are far more sensitive than our backs. We simply don’t need to make fine discriminations with our backs. But we use our hands for all sorts of things–like picking up objects or using tools–that demand that sort of sensory power.
Keyword: Pain & Touch
Link ID: 18407 - Posted: 07.25.2013
By SABRINA TAVERNISE WASHINGTON — The Food and Drug Administration announced on Monday that it had approved the first brain wave test to help diagnose attention deficit hyperactivity disorder in children. The test uses an electroencephalogram, or EEG, with sensors attached to a child’s head and hooked by wires to a computer to measure brain waves. It traces different types of electrical impulses given off by nerve cells in the brain and records how many times those impulses are given off each second. The test takes 15 to 20 minutes, and measures two kinds of brain waves — theta and beta. Certain combinations of those waves tend to be more prevalent in children with A.D.H.D., the Food and Drug Administration said in a news release. The disorder is one of the most common behavioral disorders in children. About 9 percent of adolescents have A.D.H.D. and the average age of diagnosis is 7, the drug agency said, citing the American Psychiatric Association. Children who have it tend to be hyperactive, impulsive and exhibit behavioral problems. The maker of the testing device, NEBA Health of Augusta, Ga., gave the F.D.A. data from a study of 275 children and adolescents, ages 6 to 17, with attention or hyperactivity problems. Clinicians used the device, called a Neuropsychiatric EEG-Based Assessment Aid, in combination with traditional testing methods, like listing the criteria in the Diagnostic and Statistical Manual of Mental Disorders, behavioral questionnaires and I.Q. testing. An outside group of researchers then reviewed the data and decided whether the child had the disorder. The results showed that the device helped doctors make a more accurate diagnosis than using traditional methods alone, the F.D.A. said. An agency spokeswoman said it did not release the study’s data. © 2013 The New York Times Company
Link ID: 18380 - Posted: 07.16.2013
Gregory Gage is being honored as a Champion of Change for his dedication to increasing public engagement in science and science literacy. Science has a rich history of everyday citizens assisting in great discoveries, and I am honored that our work to encourage amateur neuroscience has been selected by The White House for the Citizen Science Champion of Change award. We know a lot about how our amazing brain works, but there is much, much more that remains to be discovered. In fact, we have no cures and only insufficient treatments for neurological disorder, even though about 1 out of every 5 people will be diagnosed with a brain disease. Change is indeed needed in our nation’s approach to science education to bring more focus on neuroscience. I am a “DIY” neuroscientist. I co-founded a low-fi company called Backyard Brains with my grad-school labmate, Tim Marzullo. While working on our Ph.D., we would often go out to local public schools to talk about the importance of studying neuroscience. We developed our lesson plans using models and analogies about how the brain works, but what we really wanted to teach the students was “electrophysiology”... as this is truly is how the brain works. The brain is an electrical organ, and the cells (neurons) communicate with “spikes”: a brief pulse of electricity. In my research at the university, I would record these spikes to learn what the neurons were telling us about how the brain worked. Traditionally, to do experiments with electrophysiology, one needs to be in a Ph.D. program and use expensive equipment (our electrophysiology rig cost $40,000). To make this accessible for our outreach goals, Tim and I set out on a self-imposed engineering challenge: to reduce this equipment down to the basic components, and record a spike for <$100. Less than a year later, we got our first prototype to work and were able to bring spikes into the classrooms! After getting requests from colleagues and teachers, we launched Backyard Brains. We are now a growing education company with neuroscience gear in over 45 countries on all 7 continents!
Link ID: 18349 - Posted: 07.06.2013
by Anil Ananthaswamy Name: Sandra Condition: Ecstatic epilepsy "It's like when you have an orgasm. You don't get to the orgasm in one step. You go progressively. [My seizure] was the same kind of thing." Sandra thinks she had her earliest epileptic seizures when she was just 4 years old. But they were no ordinary seizures. Hers gave her an intense feeling of bliss. Blissful is not how most of us think of epilepsy. Fabienne Picard at the University Hospital Geneva, in Switzerland, says Sandra experienced a form of partial seizure – one localised to a specific region of the brain – known as an ecstatic seizure. These were immortalised in literature by the Russian novelist Fyodor Dostoevsky, who also had them. Dostoevsky described his seizures in a letter to a friend: "I feel entirely in harmony with myself and the whole world, and this feeling is so strong and so delightful that for a few seconds of such bliss one would gladly give up 10 years of one's life, if not one's whole life." To explain how she felt during her seizures, Sandra makes an analogy with a highly pleasurable event. "It's like when you have an orgasm," she says. "You don't get to the orgasm in one step. You go progressively. [The seizure] was the same kind of thing." However, "it was not a sexual feeling", she says. "It was more psychological." © Copyright Reed Business Information Ltd.
Link ID: 18298 - Posted: 06.22.2013
by Alyssa Danigelis Next time you happen across an enormous cockroach, check to see whether it’s got a backpack on. Then look for the person controlling its movements with a phone. The RoboRoach has arrived. The RoboRoach is a system created by University of Michigan grads who have backgrounds in neuroscience, Greg Gage and Tim Marzullo. They came up with the cyborg roach idea as part of an effort to show students what real brain spiking activity looks like using off-the-shelf electronics. Essentially the RoboRoach involves taking a real live cockroach, putting it under anesthesia and placing wires in its antenna. Then the cockroach is outfitted with a special lightweight little backpack Gage and Marzullo developed that sends pulses to the antenna, causing the neurons to fire and the roach to think there’s a wall on one side. So it turns. The backpack connects to a phone via Bluetooth, enabling a human user to steer the cockroach through an app. Why? Why would anyone do this? ”We want to create neural interfaces that the general public can use,” the scientists say in a video. “Typically, to understand how these hardware devices and biological interfaces work, you’d have to go to graduate school in a neuro-engineering lab.” They added that the product is a learning tool, not a toy, and through it they hope to start a neuro-revolution. Currently the duo’s Backyard Brains startup is raising money through a Kickstarter campaign to develop more fine-tuned prototypes, make them more affordable, and extend battery life. The startup says it will make the RoboRoach hardware by hand in an Ann Arbor hacker space. © 2013 Discovery Communications, LLC
Link ID: 18264 - Posted: 06.12.2013
Kerri Smith Researchers have both created and relieved symptoms of obsessive-compulsive disorder (OCD) in genetically modified mice using a technique that turns brain cells on and off with light, known as optogenetics. The work, by two separate teams, confirms the neural circuits that contribute to the condition and points to treatment targets. It also provides insight into how quickly compulsive behaviours can develop — and how quickly they might be soothed. The results of the studies are published in Science1, 2. Brain scanning in humans with OCD has pointed to two areas — the orbitofrontal cortex, just behind the eyes, and the striatum, a hub in the middle of the brain — as being involved in the condition's characteristic repetitive and compulsive behaviours. But “in people we have no way of testing cause and effect”, says Susanne Ahmari, a psychiatrist and neuroscientist at Columbia University in New York who led one of the studies. It is not clear, for example, whether abnormal brain activity causes the compulsions, or whether the behaviour simply results from the brain trying to hold symptoms at bay by compensating. “There’s been a big debate in the field,” says Satinder Kaur Singh of Yale University in New Haven, Connecticut, who studies molecules involved in OCD-like disorders but was not involved in the new studies. “What the Ahmari paper shows is that it is causative.” © 2013 Nature Publishing Group
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18248 - Posted: 06.08.2013
By James Gallagher Health and science reporter, BBC News An experimental treatment to stop the body attacking its own nervous system in patients with multiple sclerosis (MS) appears safe in trials. The sheath around nerves cells, made of myelin, is destroyed in MS, leaving the nerves struggling to pass on messages. A study on nine patients, reported in Science Translational Medicine, tried to train the immune system to cease its assault on myelin. The MS Society said the idea had "exciting potential". As nerves lose their ability to talk to each other, the disease results in problems moving and balancing and can affect vision. There are drugs that can reduce number and severity of attacks, but there is no cure. The disease is caused by the body's immune system thinking that myelin is a foreign body like a flu virus. Researchers at the Northwestern University Feinberg School of Medicine developed a technique to retrain the immune system. They took blood samples and coupled white blood cells, a part of the immune system, to fragments of myelin. This was injected back into the patients to make them tolerate myelin. BBC © 2013
By Geoffrey Mohan Hyperactive brain cells firing together could be an early indicator of autism and developmental disabilities, a team of UCLA researchers has found. Networks of neurons were found to be firing in a highly synchronized and seemingly unrelenting fashion, even through sleep, in the brains of juvenile mice that have a genetic abnormality similar to one that causes mental retardation and autism symptoms in humans, according to the research published online Monday in Nature Neuroscience. Without independently firing neurons, the human brain would be about as functionally complicated as a digital switch. With it, we compose poetry and send robotic carts to Mars. "If you want to code information, you can’t just have all the cells fire together or not, because then that’s just binary. It goes up and down," said UCLA neuroscientist Carlos Portera-Cailliau, a lead author of the report. “But if you have billions of neurons, all firing independently or in small clusters, then you can code a lot of information.” That “de-synchronization” was greatly diminished in the neocortex of the juvenile mice that had been altered so that they lack the same protein known to cause mental retardation and autistic behaviors in humans. These so-called Fmr1 Knockout mice, named for the gene that is knocked out, exhibit autism behaviors, among them social deficits – they don’t go over and sniff and examine a new mouse introduced to the cage, like wild mice would. Copyright 2013
Link ID: 18235 - Posted: 06.05.2013
Kerri Smith When Karl Deisseroth moved into his first lab in 2004, he found himself replacing a high-profile tenant: Nobel-prizewinning physicist Steven Chu. “His name was still on the door when I moved in,” says Deisseroth, a neuroscientist, of the basement space at Stanford University in California. The legacy has had its benefits. When chemistry student Feng Zhang dropped by looking for Chu, Deisseroth convinced him to stick around. “I don't think he knew who I was. But he got interested enough.” Deisseroth is now a major name in science himself. He is associated with two blockbuster techniques that allow researchers to show how intricate circuits in the brain create patterns of behaviour. The development of the methods, he says, came from a desire to understand mechanisms that give rise to psychiatric disease — and from the paucity of techniques to do so. “It was extremely clear that for fundamental advances in these domains I would have to spend time developing new tools,” says Deisseroth. His measured tone and laid-back demeanour belie the frenzy that his lab's techniques are generating in neuroscience. First came optogenetics1, which involves inserting light-sensitive proteins from algae into neurons, allowing researchers to switch the cells on and off with light. Deisseroth developed the method shortly after starting his lab, working with Zhang and Edward Boyden, a close collaborator at the time. Optogenetics has since been adopted by scientists around the world to explore everything from the functions of neuron subtypes to the circuits altered in depression or autism. Deisseroth has lost count of how many groups are using it. “We sent clones to thousands of laboratories,” he says. © 2013 Nature Publishing Group
Keyword: Brain imaging
Link ID: 18210 - Posted: 05.30.2013
By Nathan Seppa Multiple sclerosis, long considered a disease of white females, has affected more black women in recent years, a new study finds. Hispanic and Asian women, who have previously seemed to be at less risk of MS, remain so, researchers report May 7 in Neurology. The findings bolster a theory that vitamin D deficiency, which is common in people with dark skin in northern latitudes, contributes to MS. MS is a debilitating condition in which the protective coatings on nerves in the central nervous system get damaged, resulting in a loss of motor control, muscle weakness, vision complications and other problems. The National Multiple Sclerosis Society estimates that 2.1 million people worldwide have the condition. The researchers scanned medical information from 3.5 million people who were members of the health maintenance organization Kaiser Permanente Southern California and found that 496 people received diagnoses of MS from 2008 through 2010. Of these patients, women comprised 70 percent, not an unusual fraction for people with MS. Surprisingly, the patients included 84 black women. That means the annual incidence of MS in black women was 10.2 cases per 100,000 people. That’s not a great risk for an individual, but it was higher than the annual rates for white, Hispanic and Asian women, which were 6.9, 2.9 and 1.4 per 100,000 people, respectively. Among blacks, women had three times the incidence as men; in the other racial and ethnic groups, the MS rate in women was roughly double that of men. © Society for Science & the Public 2000 - 2013