Chapter 5. The Sensorimotor System
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It takes a lot to deter a male from wanting sex. A new study has found that male mice keep trying to copulate even when they are in pain, whereas females engage in less sex. But when given drugs that target pleasure centers in the human brain, the females again became interested. The findings could shed light on the nature of libido across various animal species. To assess how pain influences sexual desire, researchers first identified pairs of mice that wanted to have sex. “What we found early on was not all mice will mate with each other,” says clinical psychologist Melissa Farmer, who led the study while earning her Ph.D. at McGill University in Montreal, Canada. The team set up the rodents on a series of “dates,” during which a male and female were paired together for 30 minutes. Couples that copulated for most of the session were deemed compatible and moved into a cage with separate rooms. A small doorway allowed a female mouse to freely cross over from her chamber, but the male—which is larger—could not. The scientists then induced pain in males or females by applying a small dose of inflammatory compounds to the cheek, tail, foot, or genitals. The sensation would primarily be soreness, like a bad sunburn, says Farmer, who now works at Northwestern University’s Feinberg School of Medicine in Chicago, Illinois. Female mice that were in pain, whether genital or nongenital, spent 50% less time with their male partners, implying a decrease in sexual motivation. Even when they did visit their paramours, females wouldn’t allow males to mount them with the same frequency, the team reports online today in The Journal of Neuroscience. © 2014 American Association for the Advancement of Science.
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
By SABRINA TAVERNISE Federal health regulators approved a drug overdose treatment device on Thursday that experts say will provide a powerful lifesaving tool in the midst of a surging epidemic of prescription drug abuse. Similar to an EpiPen used to stop allergic reactions to bee stings, the easy-to-use injector — small enough to tuck into a pocket or a medicine cabinet — can be used by the relatives or friends of people who have overdosed. The hand-held device, called Evzio, delivers a single dose of naloxone, a medication that reverses the effects of an overdose, and will be used on those who have stopped breathing or lost consciousness from an opioid drug overdose. Naloxone is the standard treatment in such circumstances, but until now, has been available mostly in hospitals and other medical settings, when it is often used too late to save the patient. The decision to quickly approve the new treatment, which is expected to be available this summer, comes as deaths from opioids continue to mount, including an increase in those from heroin, which contributed to the death of the actor Philip Seymour Hoffman in February. Federal health officials, facing criticism for failing to slow the rising death toll, are under pressure to act, experts say. “This is a big deal, and I hope gets wide attention,” said Dr. Carl R. Sullivan III, director of the addictions program at West Virginia University. “It’s pretty simple: Having these things in the hands of people around drug addicts just makes sense because you’re going to prevent unnecessary mortality.” The scourge of drug abuse has battered states across the country, with deaths from overdoses now outstripping those from traffic crashes. Prescription drugs alone now account for more than half of all drug overdose deaths, and one major category of them, opioids, or painkillers, take the lives of more Americans than heroin and cocaine combined. Deaths from opioids have quadrupled in 10 years to more than 16,500 in 2010, according to federal data. © 2014 The New York Times Company
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 Andy Coghlan Burmese pythons can find their way home even if they are taken dozens of kilometres away. It is the first demonstration that big snakes can navigate at all, and far exceeds the distances known to have been travelled by any other snake. At over 3 metres long, Burmese pythons (Python molurus bivitattus) are among the world's largest snakes. For the last two decades they have been eating their way through native species of Florida's Everglades National Park, having been abandoned to the wild by former owners. "Adult Burmese pythons were able to navigate back to their capture locations after having been displaced by between 21 and 36 kilometres," says Shannon Pittman of Davidson College in North Carolina. Pittman and her colleagues caught 12 pythons and fitted them with radiofrequency tags (see video). She released half of them where they were caught, as controls, and transported the other six to distant locations before releasing them. Five pythons made it back to within 5 kilometres of their capture location, and the sixth at least moved in the right direction. The displaced snakes made progress towards their destination most days and seldom strayed more than 22 degrees from the correct path. They kept this up for 94 to 296 days. By contrast, the control snakes moved randomly. On average, displaced snakes travelled 300 metres each day, while control snakes averaged just 100 metres per day. © Copyright Reed Business Information Ltd.
Keyword: Animal Migration
Link ID: 19380 - Posted: 03.19.2014
By Ella Davies Reporter, BBC Nature The whales are known for their tusks which can reach 2.6m (9ft) in length, earning them comparisons with mythological unicorns. The tusk is an exaggerated front tooth and scientists have discovered that it helps the animals sense changes in their environment. Dr Martin Nweeia from the Harvard School of Dental Medicine, US, undertook the study alongside an international team of colleagues. Through the years, many theories have tried to explain the function of the narwhal's impressive tusk. "People have said it's everything from an ice pick to an acoustic probe, but this is the first time that someone has discovered sensory function and has the science to show it," said Dr Nweeia. More recently, experts have agreed that the tusk is a sexual characteristic because it is more often exhibited by males and they appear to use them during fights to assert their social hierarchy. But because the animals are rarely seen, the exact function of the tusk has remained a mystery. Previous studies have revealed that the animals have no enamel on their tusk - the external layer of the tooth that provides a barrier in most mammal teeth. Dr Nweeia and the team's analysis revealed that the outer cementum layer of the tusk is porous and the inner dentin layer has microscopic tubes that channel in towards the centre. In the middle of the tusk lies the pulp, where nerve endings which connect to the narwhal's brain are found. BBC © 2014
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
By Neuroskeptic A neuroscience paper published before Christmas drew my eye with the expansive title: “How Thoughts Give Rise to Action“ Subtitled “Conscious Motor Intention Increases the Excitability of Target-Specific Motor Circuits”, the article’s abstract was no less bold, concluding that: These results indicate that conscious intentions govern motor function… until today, it was unclear whether conscious motor intention exists prior to movement, or whether the brain constructs such an intention after movement initiation. The authors, Zschorlich and Köhling of the University of Rostock, Germany, are weighing into a long-standing debate in philosophy, psychology, and neuroscience, concerning the role of consciousness in controlling our actions. To simplify, one school of thought holds that (at least some of the time), our intentions or plans control our actions. Many people would say that this is what common sense teaches us as well. But there’s an alternative view, in which our consciously-experienced intentions are not causes of our actions but are actually products of them, being generated after the action has already begun. This view is certainly counterintuitive, and many find it disturbing as it seems to undermine ‘free will’. That’s the background. Zschorlich and Köhling say that they’ve demonstrated that conscious intentions do exist, prior to motor actions, and that these intentions are accompanied by particular changes in brain activity. They claim to have done this using transcranial magnetic stimulation (TMS), a way of causing a localized modulation of brain electrical activity.
Link ID: 19370 - Posted: 03.17.2014
New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die. The particular mutation, in the C9orf72 gene, is the most common cause for amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), and frontotemporal degeneration (FTD), the second most common type of dementia in people under 65. This research by Jiou Wang, Ph.D., and his colleagues at Johns Hopkins University (JHU) was published in Nature and was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS). In ALS, the muscle-activating neurons in the spinal cord die, eventually causing paralysis. In FTD neurons in particular brain areas die leading to progressive loss of cognitive abilities. The mutation may also be associated with Alzheimer’s and Huntington’s diseases. DNA contains a person’s genetic code, which is made up of a unique string of bases, chemicals represented by letters. Portions of this code are divided into genes that provide instructions for making molecules (proteins) that control how cells function. The normal C9orf72 gene contains a section of repeating letters; in most people, this sequence is repeated two to 25 times. In contrast, the mutation associated with ALS and FTD can result in up to tens of thousands of repeats of this section.
Daniel Cressey Researchers have called for a common method of killing zebrafish used in laboratories to be abandoned amid growing evidence that it causes unnecessary suffering. The anaesthetic MS-222, which can be added to tanks to cause overdose, seems to distress the fish, two separate studies have shown. The studies’ authors propose that alternative anaesthetics or methods should be used instead. “These two studies — carried out independently — use different methodologies to reach the same conclusion: zebrafish detect and avoid MS-222 in the water,” says Stewart Owen, a senior environmental scientist at AstraZeneca’s Brixham Environmental Laboratory in Brixham, UK, and a co-author of one of the studies. “As this is a clear aversive response, as a humane choice, one would no longer use this agent for routine zebrafish anaesthesia.” The use of zebrafish (Danio rerio) in research has skyrocketed in recent years as scientists have sought alternatives to more controversial animal models, such as mammals. The fish are cheap and easy to keep, and although no firm data on numbers have been collected, millions are known to be housed in laboratories around the world. Nearly all will eventually be killed. MS-222 (ethyl 3-aminobenzoate methanesulphate, also known as TMS) is one of the agents most frequently used to kill the creatures. It is listed as an acceptable method of euthanasia by many institutions, and also by societies such as the American Veterinary Medical Association. But the study by Owen and his co-authors, published last year (G. D. Readman et al. PLoS ONE 8, e73773; 2013), and the second study, published earlier this month by Daniel Weary and his colleagues at the University of British Columbia in Vancouver, Canada (D. Wong et al. PLoS ONE 9, e88030; 2014), show that zebrafish seem to find the chemical distressing. The research should fundamentally change the practice, say the authors of both papers. © 2014 Nature Publishing Group
Keyword: Pain & Touch
Link ID: 19294 - Posted: 02.26.2014
By Michelle Roberts Health editor, BBC News online Doctors have devised a new way to treat amputees with phantom limb pain. Using computer-generated augmented reality, the patient can see and move a virtual arm controlled by their stump. Electric signals from the muscles in the amputated limb "talk" to the computer, allowing real-time movement. Amputee Ture Johanson says his pain has reduced dramatically thanks to the new computer program, which he now uses regularly in his home. He now has periods when he is free of pain and he is no longer woken at night by intense periods of pain. Mr Johanson, who is 73 and lives in Sweden, lost half of his right arm in a car accident 48 years ago. After a below-elbow amputation he faced daily pain and discomfort emanating from his now missing arm and hand. Over the decades he has tried numerous therapies, including hypnosis, to no avail. Within weeks of starting on the augmented reality treatment in Max Ortiz Catalan's clinic at Chalmers University of Technology, his pain has now eased. "The pain is much less now. I still have it often but it is shorter, for only a few seconds where before it was for minutes. BBC © 2014