Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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Jessica Wright A tiny fiber-optic probe inserted into the reward center of the mouse brain monitors how the mouse feels about meeting a peer — or a golf ball. The unpublished technique was presented last week at the at the 2013 Society for Neuroscience annual meeting in San Diego. Mice feel the most satisfaction when sniffing another mouse’s rear and when walking away from a golf ball, the study found. The new technique is one of only a few ways to read the electrical activity of neurons in freely moving mice and is the most noninvasive, making it ideal for monitoring social interactions. The method takes advantage of a fluorescent molecule that lights up only in the presence of calcium, which rushes into the cell when neurons fire. The researchers used mice engineered to express this molecule only in neurons that make dopamine — the chemical messenger that mediates a sense of reward — in the ventral tegmental area (VTA). The researchers placed the cable in the VTA, the source of most of the brain’s dopamine neurons. The fiber-optic cable is 400 micrometers in diameter, and could probably be half that size, says Lisa Gunaydin, who developed the method as a graduate student in Karl Deisseroth’s lab at Stanford University in California. When neurons expressing the fluorescent molecule fire, the cable reads these as a series of spikes. In the study, the researchers gave thirsty mice sweet water and, as expected, their dopamine activity in the VTA spiked each time they drank. When the mice interact with a new mouse, or a golf ball, the dopamine neurons fire more on the first encounter but dull with repeated visits, suggesting that the mice are most excited by novelty. © Copyright 2013 Simons Foundation
Keyword: Drug Abuse
Link ID: 18949 - Posted: 11.21.2013
Helen Shen Long used to treat movement disorders, deep-brain stimulation (DBS) is rapidly emerging as an experimental therapy for neuropsychiatric conditions including depression, Tourette’s syndrome, obsessive–compulsive disorder and even Alzheimer’s disease. But despite some encouraging results in patients, it remains largely unknown how the electrical pulses delivered by implants deep within the brain affect neural circuits and change behaviour. Now there is a prototype DBS device that could provide some answers, researchers reported on 10 November at the Society for Neuroscience’s annual meeting in San Diego, California. Called Harmoni, the device is the first DBS implant to monitor electrical and chemical responses in the brain while delivering electrical stimulation. “That’s new data that we haven’t really had access to in humans before,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio, who is not involved in the work. Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project. The results come at a time of great excitement in the DBS field. Last month, the US government's Defense Advanced Research Projects Agency (DARPA) announced a 5-year, US$70-million initiative to support development of the next generation of therapeutic brain-stimulating technologies. © 2013 Nature Publishing Group,
Link ID: 18922 - Posted: 11.13.2013
M. Mitchell Waldrop Kwabena Boahen got his first computer in 1982, when he was a teenager living in Accra. “It was a really cool device,” he recalls. He just had to connect up a cassette player for storage and a television set for a monitor, and he could start writing programs. But Boahen wasn't so impressed when he found out how the guts of his computer worked. “I learned how the central processing unit is constantly shuffling data back and forth. And I thought to myself, 'Man! It really has to work like crazy!'” He instinctively felt that computers needed a little more 'Africa' in their design, “something more distributed, more fluid and less rigid”. Today, as a bioengineer at Stanford University in California, Boahen is among a small band of researchers trying to create this kind of computing by reverse-engineering the brain. The brain is remarkably energy efficient and can carry out computations that challenge the world's largest supercomputers, even though it relies on decidedly imperfect components: neurons that are a slow, variable, organic mess. Comprehending language, conducting abstract reasoning, controlling movement — the brain does all this and more in a package that is smaller than a shoebox, consumes less power than a household light bulb, and contains nothing remotely like a central processor. To achieve similar feats in silicon, researchers are building systems of non-digital chips that function as much as possible like networks of real neurons. Just a few years ago, Boahen completed a device called Neurogrid that emulates a million neurons — about as many as there are in a honeybee's brain. And now, after a quarter-century of development, applications for 'neuromorphic technology' are finally in sight. © 2013 Nature Publishing Group
By Bradley E. Alger, Ph.D. Cannabis, derived from a plant and one of the oldest known drugs, has remained a source of controversy throughout its history. From debates on its medicinal value and legalization to concerns about dependency and schizophrenia, cannabis (marijuana, pot, hashish, bhang, etc.) is a hot button for politicians and pundits alike. Fundamental to understanding these discussions is how cannabis affects the mind and body, as well as the body’s cells and systems. How can something that stimulates appetite also be great for relieving pain, nausea, seizures, and anxiety? Whether its leaves and buds are smoked, baked into pastries, processed into pills, or steeped as tea and sipped, cannabis affects us in ways that are sometimes hard to define. Not only are its many facets an intrinsically fascinating topic, but because they touch on so many parts of the brain and the body, their medical, ethical, and legal ramifications are vast. The intercellular signaling molecules, their receptors, and synthetic and degradative enzymes from which cannabis gets its powers had been in place for millions of years by the time humans began burning the plants and inhaling the smoke. Despite records going back 4,700 years that document medicinal uses of cannabis, no one knew how it worked until 1964. That was when Yechiel Gaoni and Raphael Mechoulam1 reported that the main active component of cannabis is tetrahydrocannabinol (THC). THC, referred to as a “cannabinoid” (like the dozens of other unique constituents of cannabis), acts on the brain by muscling in on the intrinsic neuronal signaling system, mimicking a key natural player, and basically hijacking it for reasons best known to the plants. Since the time when exogenous cannabinoids revealed their existence, the entire natural complex came to be called the “endogenous cannabinoid system,” or “endocannabinoid system” (ECS). Copyright 2013 The Dana Foundation
Keyword: Drug Abuse
Link ID: 18874 - Posted: 11.06.2013
by Anil Ananthaswamy THE first clinical trial aimed at boosting social skills in people with autism using magnetic brain stimulation has been completed – and the results are encouraging. "As a first clinical trial, this is an excellent start," says Lindsay Oberman of the Beth Israel Deaconess Medical Centre in Boston, who was not part of the study. People diagnosed with autism spectrum disorder often find social interactions difficult. Previous studies have shown that a region of the brain called the dorsomedial prefrontal cortex (dmPFC) is underactive in people with autism. "It's also the part of the brain linked with understanding others' thoughts, beliefs and intentions," says Peter Enticott of Monash University in Melbourne, Australia. Enticott and his colleagues wondered whether boosting the activity of the dmPFC using repetitive transcranial magnetic stimulation (rTMS), which involves delivering brief but strong magnetic pulses through the scalp, could help individuals with autism deal with social situations. So the team carried out a randomised, double-blind clinical trial – the first of its kind – involving 28 adults diagnosed with either high-functioning autism or Asperger's syndrome. Some participants received 15 minutes of rTMS for 10 days, while others had none, but experienced all other aspects, such as having coils placed on their heads and being subjected to the same sounds and vibrations. © Copyright Reed Business Information Ltd.
Link ID: 18863 - Posted: 11.02.2013
/ by Charles Choi, LiveScience Using lasers, scientists can now surgically blast holes thinner than a human hair in the heads of live fruit flies, allowing researchers to see how the flies' brains work. Microscopically peering into living animals can help scientists learn more about key details of these animals' biology. For instance, tiny glass windows surgically implanted into the sides of living mice can help researchers study how cancers develop in real time and evaluate the effectiveness of potential medicines. Surgically preparing small live animals for such "intravital microscopy" is often time-consuming and requires considerable skill and dexterity. Now, Supriyo Sinha, a systems engineer at Stanford University in California, and his colleagues have developed a way to prepare live animals for such microscopy that is both fast -- taking less than a second -- and largely automated. To conduct this procedure, scientists first cooled fruit flies to anesthetize them. Then, the researchers carefully picked up the insects with tweezers and glued them to the tops of glass fibers in order to immobilize the flies' bodies and heads. Then, using a high-energy pulsed ultraviolet laser, the researchers blasted holes measuring 12 to 350 microns wide in the flies' heads. (In comparison, the average human hair is about 100 microns wide.) They then applied a saline solution to exposed tissue to help keep the fly brains healthy. © 2013 Discovery Communications, LLC.
Link ID: 18861 - Posted: 11.02.2013
By KATE MURPHY Whether it’s hitting a golf ball, playing the piano or speaking a foreign language, becoming really good at something requires practice. Repetition creates neural pathways in the brain, so the behavior eventually becomes more automatic and outside distractions have less impact. It’s called being in the zone. But what if you could establish the neural pathways that lead to virtuosity more quickly? That is the promise of transcranial direct current stimulation, or tDCS — the passage of very low-level electrical current through targeted areas of the brain. Several studies conducted in medical and military settings indicate tDCS may bring improvements in cognitive function, motor skills and mood. Some experts suggest that tDCS might be useful in the rehabilitation of patients suffering from neurological and psychological disorders, perhaps even in reducing the time and expense of training healthy people to master a skill. But the research is preliminary, and now there is concern about a growing do-it-yourself community, many of them video gamers, who are making tDCS devices with nine-volt batteries to essentially jump-start their brains. “If tDCS is powerful enough to do good, you have to wonder if, done incorrectly, it could cause harm,” said Dr. H. Branch Coslett, chief of the cognitive neurology section at the University of Pennsylvania School of Medicine and a co-author of studies showing that tDCS improves recall of proper names, fosters creativity and improves reading efficiency. Even the tDCS units used in research are often little more than a nine-volt battery with two electrodes and a controller for setting the current and the duration of the session. Several YouTube videos show how to make a rough facsimile. © 2013 The New York Times Company
Link ID: 18848 - Posted: 10.29.2013
by Tina Hesman Saey BOSTON — A variant in a gene involved in breaking down chemicals in smoke triples a smoker’s risk of multiple sclerosis, a study shows. Smoking increases by 30 to 50 percent a person’s risk of multiple sclerosis, a disease in which the immune system attacks a waxy coating around nerve cells. Scientists don’t know exactly how smoking contributes to the disease. Farren Briggs of the University of California, Berkeley and his colleagues searched DNA of thousands of people in Northern California, Norway and Sweden for genetic variants associated with both smoking and multiple sclerosis. The team found hundreds of variants in three genes involved in breaking down chemicals found in smoke, Briggs said October 24 at the annual meeting of the American Society of Human Genetics. In particular, people who smoke and who have two copies of a variant in the NAT1 gene have a risk of getting MS that is three times higher than that of smokers without the variant. For nonsmokers, the variant doesn’t increase MS risk. Citations F.B.S. Briggs et al. NAT1 in an important genetic effect modifier of tobacco smoke exposure in multiple sclerosis susceptibility in 5,453 individuals. American Society of Human Genetics annual meeting, Boston, October 24, 2013. Further Reading N. Seppa. Old drug may have new trick. Science News. Vol. 184, November 2, 2013, p. 16. N. Seppa. Black women may have highest multiple sclerosis rates. Science News. Vol. 183, June 15, 2013, p. 15. © Society for Science & the Public 2000 - 2013
Special Note to Teachers: The content of the following lesson plans compares the “normal” brain to a “zombie” brain. Zombies are not real but there are plenty of diseases that effect real people and students may have people in their lives who have suffered because of them. The following lessons about neuroscience have been inspired by the book, “The Zombie Autopsies”, written by Steven C. Schlozman, M.D., and are intended to compliment it. “The Zombie Autopsies” was inspired by George Romero’s 1968 cult-classic horror film “Night of the Living Dead”. These original lessons build upon each other and have an accompanying plot line where the world is fighting a zombie apocalypse and the best and the brightest young people are being trained as medical students – with a specialty in neuroscience – with the hopes that they will be able to provide a cure to this terrible epidemic and save humanity. For a richer experience have the students read the book in class and as homework (see suggested reading schedule) along with the class activities. Although the materials are organized as a unit, lessons can be used as stand-alone or can be shaped to fit the needs of you and your students regarding time and content. For example, Lesson 3 is perfect for the day of Halloween. © 2013 MacNeil-Lehrer Productions
Keyword: Learning & Memory
Link ID: 18824 - Posted: 10.23.2013
A narrowing of the veins from the brain is unlikely as a cause multiple sclerosis, say researchers from B.C. and Saskatchewan who found the narrowing is a common and normal finding in most people. Italian Paolo Zamboni made headlines in Canada four years ago for his belief that clearing blocked or narrowed neck veins could relieve MS symptoms. Since then probably more than 3,000 Canadians have gone out of country for dilation treatment, said Dr. Anthony Traboulsee of the University of British Columbia. In Tuesday's online issue of the The Lancet, Traboulsee and his co-authors published their findings on the prevalence of narrowing, known as chronic cerebrospinal venous insufficiency or CCSVI, in people with MS, their siblings and unrelated healthy controls. Using catheter venography to directly visualize veins, the researchers found three people tested positive for CCSVI: One of 65 (2 per cent) of those with MS. One of 46 (2 per cent) of siblings. One of 32 (3 per cent) on unrelated controls. "This was a big surprise to all of us," Traboulsee told reporters. "We were really expecting to find many more people with this feature." When the researchers used ultrasound to look for CCSVI, they found narrowing in more than 50 per cent of all three groups. The hypothesis that vein narrowing has a role in the cause of MS is unlikely since its prevalence was similar in all three groups, the study's authors concluded. © CBC 2013
Keyword: Multiple Sclerosis
Link ID: 18765 - Posted: 10.09.2013
At the TEDx conference in Detroit last week, RoboRoach #12 scuttled across the exhibition floor, pursued not by an exterminator but by a gaggle of fascinated onlookers. Wearing a tiny backpack of microelectronics on its shell, the cockroach—a member of the Blaptica dubia species—zigzagged along the corridor in a twitchy fashion, its direction controlled by the brush of a finger against an iPhone touch screen (as seen in video above). RoboRoach #12 and its brethren are billed as a do-it-yourself neuroscience experiment that allows students to create their own “cyborg” insects. The roach was the main feature of the TEDx talk by Greg Gage and Tim Marzullo, co-founders of an educational company called Backyard Brains. After a summer Kickstarter campaign raised enough money to let them hone their insect creation, the pair used the Detroit presentation to show it off and announce that starting in November, the company will, for $99, begin shipping live cockroaches across the nation, accompanied by a microelectronic hardware and surgical kits geared toward students as young as 10 years old. That news, however, hasn’t been greeted warmly by everyone. Gage and Marzullo, both trained as neuroscientists and engineers, say that the purpose of the project is to spur a “neuro-revolution” by inspiring more kids to join the fields when they grow up, but some critics say the project is sending the wrong message. "They encourage amateurs to operate invasively on living organisms" and "encourage thinking of complex living organisms as mere machines or tools," says Michael Allen Fox, a professor of philosophy at Queen's University in Kingston, Canada. © 2013 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 18755 - Posted: 10.08.2013
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