Chapter 11. Motor Control and Plasticity
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By MICHAEL BEHAR One morning in May 1998, Kevin Tracey converted a room in his lab at the Feinstein Institute for Medical Research in Manhasset, N.Y., into a makeshift operating theater and then prepped his patient — a rat — for surgery. A neurosurgeon, and also Feinstein Institute’s president, Tracey had spent more than a decade searching for a link between nerves and the immune system. His work led him to hypothesize that stimulating the vagus nerve with electricity would alleviate harmful inflammation. “The vagus nerve is behind the artery where you feel your pulse,” he told me recently, pressing his right index finger to his neck. The vagus nerve and its branches conduct nerve impulses — called action potentials — to every major organ. But communication between nerves and the immune system was considered impossible, according to the scientific consensus in 1998. Textbooks from the era taught, he said, “that the immune system was just cells floating around. Nerves don’t float anywhere. Nerves are fixed in tissues.” It would have been “inconceivable,” he added, to propose that nerves were directly interacting with immune cells. Nonetheless, Tracey was certain that an interface existed, and that his rat would prove it. After anesthetizing the animal, Tracey cut an incision in its neck, using a surgical microscope to find his way around his patient’s anatomy. With a hand-held nerve stimulator, he delivered several one-second electrical pulses to the rat’s exposed vagus nerve. He stitched the cut closed and gave the rat a bacterial toxin known to promote the production of tumor necrosis factor, or T.N.F., a protein that triggers inflammation in animals, including humans. “We let it sleep for an hour, then took blood tests,” he said. The bacterial toxin should have triggered rampant inflammation, but instead the production of tumor necrosis factor was blocked by 75 percent. “For me, it was a life-changing moment,” Tracey said. What he had demonstrated was that the nervous system was like a computer terminal through which you could deliver commands to stop a problem, like acute inflammation, before it starts, or repair a body after it gets sick. “All the information is coming and going as electrical signals,” Tracey said. For months, he’d been arguing with his staff, whose members considered this rat project of his harebrained. “Half of them were in the hallway betting against me,” Tracey said. © 2014 The New York Times Company
Link ID: 19649 - Posted: 05.23.2014
A drug to treat a particular form of Duchenne muscular dystrophy has been given the green light by the European Medicines Agency and could be available in the UK in six months. Translarna is only relevant to patients with a 'nonsense mutation', who make up 10-15% of those affected by Duchenne. The EMA decided not to pass the drug in January, but they have since re-examined the evidence. A campaign group said the drug must reach the right children without delay. There are currently no approved therapies available for this life-threatening condition. The patients who will benefit the most are those aged five years and over who are still able to walk, the EMA said. Duchenne muscular dystrophy is a genetic disease that gradually causes weakness and loss of muscle function. Patients with the condition lack normal dystrophin, a protein found in muscles, which helps to protect muscles from injury. In patients with the disease, the muscles become damaged and eventually stop working. There are 2,400 children in the UK living with muscular dystrophy, but only those whose condition is caused by a particular 'nonsense mutation' - namely 200 children - are suitable to use Translarna. The drug, ataluren, will be known by the brand name of Translarna in the EU. It was developed by PTC Therapeutics. The next step will see the European Commission rubberstamp the EMA's scientific 'green light' within the next three months and authorise the drug to be marketed in the European Union. At that point, individual member states, including the UK, must decide how it will be funded. The Muscular Dystrophy Campaign is calling for urgent meetings with National Institute of Health of Clinical Excellence (NICE) and NHS England to discuss how Translarna can be cleared for approval and use in the UK. It said families in the UK could have access to the drug by spring 2015. Robert Meadowcroft, chief executive of the campaign, said: "This decision by the EMA is fantastic news. BBC © 2014
By JAMES GORMAN If an exercise wheel sits in a forest, will mice run on it? Every once in a while, science asks a simple question and gets a straightforward answer. In this case, yes, they will. And not only mice, but also rats, shrews, frogs and slugs. True, the frogs did not exactly run, and the slugs probably ended up on the wheel by accident, but the mice clearly enjoyed it. That, scientists said, means that wheel-running is not a neurotic behavior found only in caged mice. They like the wheel. Two researchers in the Netherlands did an experiment that it seems nobody had tried before. They placed exercise wheels outdoors in a yard garden and in an area of dunes, and monitored the wheels with motion detectors and automatic cameras. They were inspired by questions from animal welfare committees at universities about whether mice were really enjoying wheel-running, an activity used in all sorts of studies, or were instead like bears pacing in a cage, stressed and neurotic. Would they run on a wheel if they were free? Now there is no doubt. Mice came to the wheels like human beings to a health club holding a spring membership sale. They made the wheels spin. They hopped on, hopped off and hopped back on. “When I saw the first mice, I was extremely happy,” said Johanna H. Meijer at Leiden University Medical Center in the Netherlands. “I had to laugh about the results, but at the same time, I take it very seriously. It’s funny, and it’s important at the same time.” Dr. Meijer’s day job is as a “brain electrophysiologist” studying biological rhythms in mice. She relished the chance to get out of the laboratory and study wild animals, and in a way that no one else had. © 2014 The New York Times Company
Dr. Mark Saleh Bell's palsy is a neurological condition frequently seen in emergency rooms and medical offices. Symptoms consist of weakness involving all muscles on one side of the face. About 40,000 cases occur annually in the United States. Men and women are equally affected, and though it can occur at any age, people in their 40s are especially vulnerable. The facial weakness that occurs in Bell's palsy prevents the eye of the affected side from blinking properly and causes the mouth to droop. Because the eyelid doesn't close sufficiently, the eye can dry and become irritated. Bell's palsy symptoms progress fairly rapidly, with weakness usually occurring within three days. If the progression of weakness is more gradual and extends beyond a week, Bell's palsy may not be the problem, and other potential causes should be investigated. Those with certain medical conditions, such as diabetes or pregnancy, are at greater risk of developing Bell's palsy, and those who have had one episode have an 8 percent chance of recurrence. Bell's palsy is thought to occur when the seventh cranial (facial) nerve becomes inflamed. The nerve controls the muscles involved in facial expression and is responsible for other functions, including taste perception, eye tearing and salivation. The cause of the inflammation is unknown, although the herpes simplex virus and autoimmune inflammation are possible causes. © 2014 Hearst Communications, Inc.
Keyword: Movement Disorders
Link ID: 19637 - Posted: 05.20.2014
Katia Moskvitch The hundreds of suckers on an octopus’s eight arms leech reflexively to almost anything they come into contact with — but never grasp the animal itself, even though an octopus does not always know what its arms are doing. Today, researchers reveal that the animal’s skin produces a chemical that stops the octopus’s suckers from grabbing hold of its own body parts, and getting tangled up. “Octopus arms have a built-in mechanism that prevents the suckers from grabbing octopus skin,” says neuroscientist Guy Levy at the Hebrew University of Jerusalem, the lead author of the work, which appears today in Current Biology1. It is the first demonstration of a chemical self-recognition mechanism in motor control, and could help scientists to build better bio-inspired soft robots. To find out just how an octopus avoids latching onto itself, Levy and his colleagues cut off an octopus’s arm and subjected it to a series of tests. (The procedure is not considered traumatic, says Levy, because octopuses occasionally lose an arm in nature and behave normally while the limb regenerates.) The severed arms remained active for more than an hour after amputation, firmly grabbing almost any object, with three exceptions: the former host; any other live octopus; and other amputated arms. “But when we peeled the skin off an amputated arm and submitted it to another amputated arm, we were surprised to see that it grabbed the skinned arm as any other item,” says co-author Nir Nesher, also a neuroscientist at the Hebrew University. © 2014 Nature Publishing Group,
Link ID: 19623 - Posted: 05.15.2014
By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post
by Lisa Grossman Hasta la vista, nerve damage. Experiments with bullfrog nerves show that a Terminator-style liquid metal alloy could one day be placed in the body to help severed nerves reconnect. The alloy would stay in place until the nerve has healed, before being slurped back out with a syringe. The peripheral nervous system consists of nerves that carry electrical signals from the brain to the rest of the body. Because they aren't protected by the spine or the skull, peripheral nerves are more vulnerable to injuries than those in the central nervous system. Severed nerves can reconnect if treated quickly enough, but at a rate of just 1 millimetre per day. Also, existing methodsMovie Camera for grafting nerve ends back together have serious shortcomings. For instance, most existing scaffolds for grafts must ultimately be removed, requiring risky follow-up surgery. Even more worrisome, if the nerves don't pass signals to muscles during the healing process, the muscles can atrophy to the point where they never fully recover. Liu and his colleagues wondered if liquid metal could act as a backup system for damaged nerves, helping signals pass through a graft while the nerve healed. They used an alloy of gallium, indium and selenium, which is a very good electrical conductor. The alloy is liquid at room temperature, allowing it to be removed with a syringe when it's no longer needed. © Copyright Reed Business Information Ltd.
By Julie Steenhuysen CHICAGO (Reuters) - International teams of researchers using advanced gene sequencing technology have uncovered a single genetic mutation responsible for a rare brain disorder that may have stricken families in Turkey for some 400 years. The discovery of this genetic disorder, reported in two papers in the journal Cell, demonstrates the growing power of new tools to uncover the causes of diseases that previously stumped doctors. Besides bringing relief to affected families, who can now go through prenatal genetic testing in order to have children without the disorder, the discovery helps lend insight into more common neurodegenerative disorders, such as ALS, also known as Lou Gehrig's disease, the researchers said. The reports come from two independent teams of scientists, one led by researchers at Baylor College of Medicine and the Austrian Academy of Sciences, and the other by Yale University, the University of California, San Diego, and the Academic Medical Center in the Netherlands. Both focused on families in Eastern Turkey where marriage between close relatives, such as first cousins, is common. Geneticists call these consanguineous marriages. In this population, the researchers focused specifically on families whose children had unexplained neurological disorders that likely resulted from genetic defects. Both teams identified a new neurological disorder arising from a single genetic variant called CLP1. Children born with this disorder inherit two defective copies of this gene, which plays a critical role in the health of nerve cells. Babies with the disorder have small and malformed brains, they develop progressive muscle weakness, they do not speak and they are increasingly prone to seizures.
Chelsea Wald The sailfish’s sword-like bill looks as if it was made to slash at prey. But a study published today in Proceedings of the Royal Society B1 reveals that the bill is actually a multifunctional killing tool, enabling the fish to perform delicate, as well as swashbuckling, manoeuvres. By following throngs of predatory birds off the coast of Cancún, Mexico, the study’s authors were able to track Atlantic sailfish (Istiophorus albicans) hunting sardines, says co-author Alexander Wilson, a behavioural ecologist now at Carleton University in Ottawa, Canada. He and his colleagues made high-speed, high-resolution films in the open ocean over six days in 2012. Sailfish hunt in groups, taking turns to approach the ball of schooling fish. Their bodies darken and sometimes flash stripes and spots, perhaps to confuse the prey, or to signal to each other. “It’s a very orderly process,” Wilson says. “They don’t want to risk breaking their bills.” Although sailfish are among the fastest creatures in the ocean — they have been documented to swim at more than 110 kilometres per hour, or 60 knots — the new research shows that their strategy is to approach their prey slowly from behind and gently insert their bills into the school, without eliciting an evasive manoeuvre from the sardines. Then, by whipping their heads in powerful, sudden jerks, they can slash their bills left and right, with their upright fins providing stability. In fact, their bill tips slash with about the same acceleration as the tip of a swinging baseball bat, even in the water, says co-author Paolo Domenici, an environmental physiologist at the Institute for the Marine and Coastal Environment of Italy's National Research Council in Torregrande, on the island of Sardinia. The result is a scene of fishy carnage, as the surrounding water fills with iridescent fragments of sardine skin. © 2014 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 19523 - Posted: 04.23.2014
Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. “The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development,” said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, the NIH institute that funded the study. The study is available online in the April issue of the Journal of Cell Biology. It was led by Dr. Gyorgy Hajnoczky, M.D., Ph.D., director of Thomas Jefferson University’s MitoCare Center, Philadelphia, and professor in the Department of Pathology, Anatomy and Cell Biology. Mitochondria are cellular structures that generate most of the energy needed by cells. Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion — joining with other mitochondria and exchanging material such as DNA. Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle.
By Bill Briggs A Vietnam veteran swoops his hand through a row of baby vegetables, caressing the peppers on down to the kale. The plants are aligned in tidy, military order atop his backyard fence. He could spend hours describing his first garden. But he cannot utter a word. He can’t even eat his eventual harvest. So, Bob Hoaglan, 71, simply stands and grins at the spouts behind his Oxnard, Calif., home. Then, he grabs his primary communication tool, an LCD tablet, scribbling a stylus across the screen. He displays his words with a silent chuckle: “I don’t have a green thumb.” With a button click, he erases that sentence before composing another. His daily aim is to throw his body and brain into new pursuits. The crops — fresh life for a man facing mortality — help shove his disease to the back of his mind. He admits, though, he can’t keep it there: “I try,” he writes, “Sometimes it creeps up on me.” As he shows that message, the smile vanishes. Hoaglan was diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, nearly a year ago. Inside a malady that offers no cure or explanation, he embodies two intriguing clues that, a top researcher says, may whisper answers: Hoaglan served in the military, and he is a nice man. U.S. veterans carry a nearly 60 percent greater risk of contracting ALS than civilians, according to a white paper published in 2013 by the ALS Association, citing Harvard University research that tracked ex-service members back to 1910.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 19509 - Posted: 04.19.2014
Scientists may have discovered how the most common genetic cause of Parkinson’s disease destroys brain cells and devastates many patients worldwide. The study was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS); the results may help scientists develop new therapies. The investigators found that mutations in a gene called leucine-rich repeat kinase 2 (LRRK2; pronounced “lark two” or “lurk two”) may increase the rate at which LRRK2 tags ribosomal proteins, which are key components of protein-making machinery inside cells. This could cause the machinery to manufacture too many proteins, leading to cell death. “For nearly a decade, scientists have been trying to figure out how mutations in LRRK2 cause Parkinson’s disease,” said Margaret Sutherland, Ph.D., a program director at NINDS. “This study represents a clear link between LRRK2 and a pathogenic mechanism linked to Parkinson’s disease.” Affecting more than half a million people in the United States, Parkinson’s disease is a degenerative disorder that attacks nerve cells in many parts of the nervous system, most notably in a brain region called the substantia nigra, which releases dopamine, a chemical messenger important for movement. Initially, Parkinson’s disease causes uncontrolled movements; including trembling of the hands, arms, or legs. As the disease gradually worsens, patients lose ability to walk, talk or complete simple tasks.
Link ID: 19477 - Posted: 04.12.2014
|By Bret Stetka The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s. Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity. Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields. © 2014 Scientific American
by Clare Wilson A genetic tweak can make light work of some nervous disorders. Using flashes of light to stimulate modified neurons can restore movement to paralysed muscles. A study demonstrating this, carried out in mice, lays the path for using such "optogenetic" approaches to treat nerve disorders ranging from spinal cord injury to epilepsy and motor neuron disease. Optogenetics has been hailed as one of the most significant recent developments in neuroscience. It involves genetically modifying neurons so they produce a light-sensitive protein, which makes them "fire", sending an electrical signal, when exposed to light. So far optogenetics has mainly been used to explore how the brain works, but some groups are exploring using it as therapy. One stumbling block has been fears about irreversibly genetically manipulating the brain. In the latest study, a team led by Linda Greensmith of University College London altered mouse stem cells in the lab before transplanting them into nerves in the leg – this means they would be easier to remove if something went wrong. "It's a very exciting approach that has a lot of potential," says Ziv Williams of Harvard Medical School in Boston. Greensmith's team inserted an algal gene that codes for a light-responsive protein into mouse embryonic stem cells. They then added signalling molecules to make the stem cells develop into motor neurons, the cells that carry signals to and from the spinal cord to the rest of the body. They implanted these into the sciatic nerve – which runs from the spinal cord to the lower limbs – of mice whose original nerves had been cut. © Copyright Reed Business Information Ltd.
Keyword: Movement Disorders
Link ID: 19450 - Posted: 04.05.2014
Walking backward may seem a simple task, but researchers don’t know how the mind controls this behavior. A study published online today in Science provides the first glimpse of the brain circuit responsible—at least in fruit flies. Geneticists created 3500 strains of the insects, each with a temperature-controlled switch that turned random networks of neurons on when the flies entered an incubator. One mutant batch of fruit flies started strolling in reverse when exposed to warmth (video, right panel), which the team dubbed “moonwalkers,” in honor of Michael Jackson’s famous dance. Two neurons were responsible for the behavior. One lived in the brain and extended its connections to the end of the ventral nerve cord—the fly’s version of a spine, which runs along its belly. The other neuron had the opposite orientation—it started at the bottom of the nerve cord and sent its messaging cables—or axons—into the brain. The neuron in the brain acted like a reverse gear in a car; when turned on, it triggered reverse walking. The researchers say this neuron is possibly a command center that responds to environmental cues, such as, “Hey! I see a wall in front of me.” The second neuron functioned as the brakes for forward motion, but it couldn’t compel the fly to moonwalk. It may serve as a fail-safe that reflexively prevents moving ahead, such as when the fly accidentally steps onto a very cold floor. Using the two neurons as a starting point, the team will trace their links to sensory neurons for touch, sight, and smell, which feed into and control the moonwalking network. No word yet on the neurons responsible for the Macarena. © 2014 American Association for the Advancement of Science
Keyword: Movement Disorders
Link ID: 19445 - Posted: 04.05.2014
For years, some biomedical researchers have worried that a push for more bench-to-bedside studies has meant less support for basic research. Now, the chief of one of the National Institutes of Health’s (NIH’s) largest institutes has added her voice—and hard data—to the discussion. Story Landis describes what she calls a “sharp decrease” in basic research at her institute, a trend she finds worrisome. In a blog post last week, Landis, director of the $1.6 billion National Institute of Neurological Disorders and Stroke (NINDS), says her staff started out asking why, in the mid-2000s, NINDS funding declined for R01s, the investigator-initiated grants that are the mainstay of most labs. After examining the aims and abstracts of grants funded between 1997 and 2012, her staff found that the portion of NINDS competing grant funding that went to basic research has declined (from 87% to 71%) while applied research rose (from 13% to 29%). To dig deeper, the staffers divided the grants into four categories—basic/basic; basic/disease-focused; applied/translational; and applied/clinical. Here, the decline in basic/basic research was “striking”: It fell from 52% to 27% of new and competing grants, while basic/disease-focused has been rising (see graph). The same trend emerged when the analysts looked only at investigator-initiated grants, which are proposals based on a researcher’s own ideas, not a solicitation by NINDS for proposals in a specific area. The shift could reflect changes in science and “a natural progression of the field,” Landis writes. Or it could mean researchers “falsely believe” that NINDS is not interested in basic studies and they have a better shot at being funded if they propose disease-focused or applied studies. The tight NIH budget and new programs focused on translational research could be fostering this belief, she writes. When her staff compared applications submitted in 2008 and 2011, they found support for a shift to disease-focused proposals: There was a “striking” 21% decrease in the amount of funding requested for basic studies, even though those grants had a better chance of being funded. © 2014 American Association for the Advancement of Science.
Keyword: Movement Disorders
Link ID: 19440 - Posted: 04.02.2014
by Catherine de Lange Why wait for the doctor to see you? A smart patch attached to your skin could diagnose health problems automatically – and even administer drugs. Monitoring movement disorders such as Parkinson's disease or epilepsy relies on video recordings of symptoms and personal surveys, says Dae-Hyeong Kim at the Seoul National University in South Korea. And although using wearable devices to monitor the vital signs of patients is theoretically possible, the wearable pads, straps and wrist bands that can do this are often cumbersome and inflexible. To track the progression of symptoms and the response to medication more accurately would require devices that monitor cues from the body, store recorded data for pattern analysis and deliver therapeutic agents through the human skin in a controlled way, Kim says. So Kim and his team have developed an adhesive patch that is flexible and can be worn on the wrist like a second skin. The patch is 1 millimetre thick and made of a hydrocolloid dressing – a type of thin flexible bandage. Into it they embedded a layer of silicon nanoparticles. These silicon nanomembranes are often used for flexible electronics, and can pick up the bend and stretch of human skin and convert these into small electronic signals. The signals are stored as data in separate memory cells made from layers of gold nanoparticles. The device could be used to detect and treat tremors in people who have Parkinson's disease, or epileptic seizures, says Kim. If these movements are detected, small heaters in the patch trigger the release of drugs from silicon nanoparticles. The patch also contains temperature sensors to make sure the skin doesn't burn during the process. © Copyright Reed Business Information Ltd.
By JAMES GORMAN There are lots of reasons scientists love fruit flies, but a big one is their flying ability. These almost microscopic creatures, with minimalist nervous systems and prey to every puff of wind, must often execute millisecond aerial ballets to stay aloft. To study fly flight, scientists have to develop techniques that are almost as interesting as the flies. At Cornell University, for instance, researchers have been investigating how the flies recover when their flight is momentarily disturbed. Among their conclusions: a small group of fly neurons is solving calculus problems, or what for humans are calculus problems. To do the research, the members of Cornell team — Itai Cohen and his colleagues, including Z. Jane Wang, John Guckenheimer, Tsevi Beatus and Leif Ristroph, who is now at New York University — glue tiny magnets to the flies and use a magnetic pulse to pull them this way or that. In the language of aeronautics, the scientists disturb either the flies’ pitch (up or down), yaw (left or right) or roll, which is just what it sounds like. The system, developed by Dr. Ristroph as a graduate student in Dr. Cohen’s lab, involves both low and high tech. On the low end, the researchers snip bits of metal bristle off a brush to serve as micromagnets that they glue to the flies’ backs. At the high end, three video cameras record every bit of the flight at 8,000 frames per second, and the researchers use computers to merge the data from the cameras into a three-dimensional reconstruction of the flies’ movements that they can analyze mathematically. © 2014 The New York Times Company
Link ID: 19388 - Posted: 03.20.2014
Helen Shen For Frank Donobedian, sitting still is a challenge. But on this day in early January, he has been asked to do just that for three minutes. Perched on a chair in a laboratory at Stanford University in California, he presses his hands to his sides, plants his feet on the floor and tries with limited success to lock down the trembling in his limbs — a symptom of his Parkinson's disease. Only after the full 180 seconds does he relax. Other requests follow: stand still, lie still on the floor, walk across the room. Each poses a similar struggle, and all are watched closely by Helen Bronte-Stewart, the neuroscientist who runs the lab. “You're making history,” she reassures her patient. “Everybody keeps saying that,” replies the 73-year-old Donobedian, a retired schoolteacher, with a laugh. “But I'm not doing anything.” “Well, your brain is,” says Bronte-Stewart. Like thousands of people with Parkinson's before him, Donobedian is being treated with deep brain stimulation (DBS), in which an implant quiets his tremors by sending pulses of electricity into motor areas of his brain. Last October, a team of surgeons at Stanford threaded the device's two thin wires, each with four electrode contacts, through his cortex into a deep-seated brain region known as the subthalamic nucleus (STN). But Donobedian's particular device is something new. Released to researchers in August 2013 by Medtronic, a health-technology firm in Minneapolis, Minnesota, it is among the first of an advanced generation of neurostimulators that not only send electricity into the brain, but can also read out neural signals generated by it. On this day, Bronte-Stewart and her team have temporarily turned off the stimulating current and are using some of the device's eight electrical contacts to record abnormal neural patterns that might correlate with the tremors, slowness of movement and freezing that are hallmarks of Parkinson's disease. © 2014 Nature Publishing Group,
By Gary Marcus and Christof Koch What would you give for a retinal chip that let you see in the dark or for a next-generation cochlear implant that let you hear any conversation in a noisy restaurant, no matter how loud? Or for a memory chip, wired directly into your brain's hippocampus, that gave you perfect recall of everything you read? Or for an implanted interface with the Internet that automatically translated a clearly articulated silent thought ("the French sun king") into an online search that digested the relevant Wikipedia page and projected a summary directly into your brain? Science fiction? Perhaps not for very much longer. Brain implants today are where laser eye surgery was several decades ago. They are not risk-free and make sense only for a narrowly defined set of patients—but they are a sign of things to come. Unlike pacemakers, dental crowns or implantable insulin pumps, neuroprosthetics—devices that restore or supplement the mind's capacities with electronics inserted directly into the nervous system—change how we perceive the world and move through it. For better or worse, these devices become part of who we are. Neuroprosthetics aren't new. They have been around commercially for three decades, in the form of the cochlear implants used in the ears (the outer reaches of the nervous system) of more than 300,000 hearing-impaired people around the world. Last year, the Food and Drug Administration approved the first retinal implant, made by the company Second Sight. ©2014 Dow Jones & Company, Inc.
Link ID: 19371 - Posted: 03.17.2014