Chapter 5. The Sensorimotor System

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By Emily Underwood It is famous for robbing Lou Gehrig of his life and Stephen Hawking of his mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now, scientists are converging on an explanation, at least for a fraction of the ALS cases caused by a specific mutation. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become clogged, preventing vital molecules from passing through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9orf72—a DNA stutter in which a short nucleotide sequence, GGGGCC, is repeated hundreds to thousands of times in a gene on chromosome 9. Nor do the multiple labs reporting results this week agree on exactly what plugs those nuclear pores and how the cells die. Still, the work is “a major breakthrough” in ALS research, says Amelie Gubitz, program director of the neurodegeneration division at the National Institute of Neurological Disorders in Bethesda, Maryland. The groups worked independently, starting with different hypotheses and experimental designs, yet reached similar conclusions, making the finding more convincing. And it suggests that boosting 
traffic through nuclear pores could be a new strategy for treating some cases of ALS and frontotemporal dementia (FTD), another neurodegenerative condition C9orf72 can cause. Based on past work by their own and other groups, neuroscientists Jeff 
Rothstein and Tom Lloyd at Johns Hopkins University in Baltimore, Maryland, suspected that the long strands of excess RNA produced by C9orf72 cause neurodegeneration by binding to, and thus sequestering, key cellular proteins. The team tested the idea in fruit flies with the mutation, which display damage in the nerve cells of their eyes and in motor neurons. © 2015 American Association for the Advancement of Science

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 21349 - Posted: 08.27.2015

A placebo can make you feel a little better – and now we know how to boost the effect. Drugs based on hormones that make us more cooperative seem to enhance the placebo effect. The finding could lead to changes in the way some trials are performed. Sometimes a sugar pill can be all you need, even when you know it doesn’t contain any medicine. We’re still not entirely sure why. The brain’s natural painkillers, such as dopamine and opioids, seem to be involved, but other factors may be at work too. Evidence that a compassionate, trustworthy carer can speed recovery suggests that there is also a social dimension to the placebo effect. “This interaction between the patient and care provider seems to be based on a more complex system,” says Luana Colloca at the University of Maryland in Baltimore. Hormones that modulate our social behaviour might play a role. Last year, a team led by Ulrike Bingel of the University Duisburg-Essen in Germany, found that oxytocin – the so-called “cuddle chemical” that is thought to help us trust, bond and form relationships – seems to boost the placebo effect, at least in men. In the study, Bingel’s team applied an inert ointment to the arms of male volunteers. Half of them were told that the cream would reduce the degree of pain caused by the painfully hot stimulus subsequently applied. Men who were told that they were receiving pain relief said that the heat was less painful than those who knew that the cream was inert. When oxytocin was squirted up volunteers’ noses, the men reported being in even less pain. The team didn’t test oxytocin in women. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 21336 - Posted: 08.25.2015

By Robert F. Service Move over, poppies. In one of the most elaborate feats of synthetic biology to date, a research team has engineered yeast with a medley of plant, bacterial, and rodent genes to turn sugar into thebaine, the key opiate precursor to morphine and other powerful painkilling drugs that have been harvested for thousands of years from poppy plants. The team also showed that with further tweaks, the yeast could make hydrocodone, a widely used painkiller that is now made chemically from thebaine. “This is a major milestone,” says Jens Nielsen, a synthetic biologist at Chalmers University of Technology in Göteborg, Sweden. The work, he adds, demonstrates synthetic biology’s increasing sophistication at transferring complex metabolic pathways into microbes. By tweaking the yeast pathways, medicinal chemists may be able to produce more effective, less addictive versions of opiate painkillers. But some biopolicy experts worry that morphinemaking yeast strains could also allow illicit drugmakers to brew heroin as easily as beer enthusiasts home brew today—the drug is a simple chemical conversion from morphine. That concern is one reason the research team, led by Christina Smolke, a synthetic biologist at Stanford University in Palo Alto, California, stopped short of making a yeast strain with the complete morphine pathway; medicinal drug
makers also primarily use thebaine to make new compounds. Synthetic biologists had previously engineered yeast to produce artemisinin, an antimalarial compound, but that required inserting just a handful of plant genes. To get yeast to make thebaine, © 2015 American Association for the Advancement of Science.

Keyword: Drug Abuse; Pain & Touch
Link ID: 21297 - Posted: 08.15.2015

A healthy motor neuron needs to transport its damaged components from the nerve-muscle connection all the way back to the cell body in the spinal cord. If it cannot, the defective components pile up and the cell becomes sick and dies. Researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) have learned how a mutation in the gene for superoxide dismutase 1 (SOD1), which causes ALS, leads cells to accumulate damaged materials. The study, published in the journal Neuron, suggests a potential target for treating this familial form of ALS. More than 12,000 Americans have ALS, also known as Lou Gehrig’s disease, and roughly 5-10 percent of them inherited a genetic mutation from a parent. These cases of familial ALS are often caused by mutations in the gene that codes for SOD1, an important enzyme located in the neuron’s mitochondria, the cell’s energy-producing structures. This mutation causes the death of motor neurons that control the patient’s muscles, resulting in progressive paralysis. “About 90 percent of the energy in the brain is generated by mitochondria,” said Zu-Hang Sheng, Ph.D., an NINDS scientist and the study’s senior author. “If the mitochondria aren’t healthy, they produce energy less efficiently; they can also release harmful chemicals called reactive oxygen species that cause cell death. As a consequence, mitochondrial damage can cause neurodegeneration.” In healthy neurons, storage containers called late endosomes collect damaged mitochondria and various destructive chemicals. A motor protein called dynein then transports the endosomes to structures called lysosomes, which use the chemicals to break down the endosomes. Dr. Sheng’s team discovered that this crucial process is faulty in nerve cells with SOD1 mutations because mutant SOD1 interferes with a critical molecule called snapin that hooks the endosome to the dynein motor protein.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 21294 - Posted: 08.13.2015

Richard Harris Hospitals have a free and powerful tool that they could use more often to help reduce the pain that surgery patients experience: music. Scores of studies over the years have looked at the power of music to ease this kind of pain; an analysis published Wednesday in The Lancet that pulls all those findings together builds a strong case. When researchers in London started combing the medical literature for studies about music's soothing power, they found hundreds of small studies suggesting some benefit. The idea goes back to the days of Florence Nightingale, and music was used to ease surgical pain as early as 1914. (My colleague Patricia Neighmond reported on one of these studies just a few months ago). Dr. Catherine Meads at Brunel University focused her attention on 73 rigorous, randomized clinical trials about the role of music among surgery patients. "As they studies themselves were small, they really didn't find all that much," Meads says. "But once we put them all together, we had much more power to find whether music worked or not." She and her colleagues now report that, yes indeed, surgery patients who listened to music, either before, during or after surgery, were better off — in terms of reduced pain, less anxiety and more patient satisfaction. © 2015 NPR

Keyword: Pain & Touch
Link ID: 21293 - Posted: 08.13.2015

Sarah Schwartz In 2011, science journalist Jon Palfreman saw a doctor about a tremor in his left hand. The doctor diagnosed Palfreman, then 60, with Parkinson’s disease. The disorder, which is newly diagnosed in 60,000 Americans each year, promised a crippling future of tremors, loss of mobility, dementia and more. Palfreman decided to use his reporting expertise to investigate how Parkinson’s disease affects the body and learn about efforts to find a cure. With Brain Storms, Palfreman follows Parkinson’s history from the careful observations of 19th century physicians to today’s cutting-edge research. Palfreman relates complex research studies as gripping medical mysteries. He describes how scientists connected Parkinson’s with the dramatic loss of the brain chemical dopamine and with tenacious protein knots called Lewy bodies that are a hallmark of the disease. Palfreman also explores treatments past and present, including the widely used drug levodopa that restores motion (sometimes uncontrollably), gene therapies, brain surgeries and promising experimental antibody treatments that attack and dissolve misfolded Parkinson’s-related proteins. Ultimately, Brain Storms is about more than Parkinson’s disease; it’s about the people living with the disorder. Palfreman describes patients who must teach themselves to walk without falling over or who freeze in place. He writes about a researcher driven to search for a cure after the disease affects his own father. © Society for Science & the Public 2000 - 2015

Keyword: Parkinsons
Link ID: 21284 - Posted: 08.12.2015

Joe Palca The sea snail Conus magus looks harmless enough, but it packs a venomous punch that lets it paralyze and eat fish. A peptide modeled on the venom is a powerful painkiller, though sneaking it past the blood-brain barrier has proved hard. The sea snail Conus magus looks harmless enough, but it packs a venomous punch that lets it paralyze and eat fish. A peptide modeled on the venom is a powerful painkiller, though sneaking it past the blood-brain barrier has proved hard. Courtesy of Jeanette Johnson and Scott Johnson Researchers are increasingly turning to nature for inspiration for new drugs. One example is Prialt. It's an incredibly powerful painkiller that people sometimes use when morphine no longer works. Prialt is based on a component in the venom of a marine snail. Prialt hasn't become a widely used drug because it's hard to administer. Mandë Holford is hoping to change that. She and colleagues explain how in their study published online Monday in the journal Scientific Reports. Holford is an associate professor of chemical biology at Hunter College in New York and on the scientific staff of the American Museum of Natural History. As is so often the case in science, her path to working on Prialt wasn't exactly a direct one. She's a chemist, and her first passion was peptides — short strings of amino acids that do things inside cells. "I started out with this love for peptides," Holford says, then laughs. "Love! Sounds weird to say you love peptides out loud." © 2015 NPR

Keyword: Pain & Touch
Link ID: 21255 - Posted: 08.04.2015

RACHEL MARTIN, HOST: Every day, according to the Centers for Disease Control, 44 Americans die because they have overdosed on prescription painkillers. The CDC calls it an epidemic, and drug companies are responding by trying to develop versions of the most addictive painkillers, opioids, that will diminish a user's physical craving for the medicine. Now, to do this, to create these less addictive drugs, pharmaceutical companies are recruiting thousands of self-identified drug users to test their products. David Crow is a reporter for the Financial Times. He's just published a big report on this, and he joins me now to talk more about it. Thanks so much for being with us. Opioids, as we mentioned, are the worst in terms of their addictive quality. These companies are trying to come up with drugs that will achieve the same painkilling effect without the addictiveness. So this is actually possible? CROW: What they're trying to do is develop a new generation of opioid painkillers that have features that make them harder to abuse. Some of the strategies that have been pursued include hard shells that make it harder to crush up the pill so that you can snort it or gumming agents that make it harder to put into a syringe so that you can inject it. And some companies are experimenting with putting different chemicals in the center of the pill that will remain dormant. But if it's tampered with, that chemical would be released, and it would counteract the effect of the opioid. They're testing these drugs on recreational drug users. And the participants go through a screening process where they have to wash out, where they don't have any opioid in their system, and also where they're given a drug called naloxone, which cuts off the effects of opioids. And at that point, if you were addicted or physically dependent, your body would show signs of withdrawal. And that is the screening process. © 2015 NPR

Keyword: Drug Abuse; Pain & Touch
Link ID: 21253 - Posted: 08.02.2015

By David Noonan Leaping through the air with ease and spinning in place like tops, ballet dancers are visions of the human body in action at its most spectacular and controlled. Their brains, too, appear to be special, able to evade the dizziness that normally would result from rapid pirouettes. When compared with ordinary people's brains, researchers found in a study published early this year, parts of dancers' brains involved in the perception of spinning seem less sensitive, which may help them resist vertigo. For millions of other people, it is their whole world, not themselves, that suddenly starts to whirl. Even the simplest task, like walking across the room, may become impossible when vertigo strikes, and the condition can last for months or years. Thirty-five percent of adults older than 39 in the U.S.—69 million people—experience vertigo at one time or another, often because of damage to parts of the inner ear that sense the body's position or to the nerve that transmits that information to the brain. Whereas drugs and physical therapy can help many, tens of thousands of people do not benefit from existing treatments. “Our patients with severe loss of balance have been told over and over again that there's nothing we can do for you,” says Charles Della Santina, an otolaryngologist who studies inner ear disorders and directs the Johns Hopkins Vestibular NeuroEngineering Laboratory. Steve Bach's nightmare started in November 2013. The construction manager was at home in Parsippany, N.J. “All of a sudden the room was whipping around like a 78 record,” says Bach, now age 57. He was curled up on the living room floor in a fetal position when his daughter found him and called 911. He spent the next five days in the hospital. © 2015 Scientific American

Keyword: Movement Disorders
Link ID: 21248 - Posted: 08.01.2015

Mo Costandi When we say that we are “in pain”, we usually mean that an injured body part is hurting us. But the phenomenon we call pain consists of more than just physical sensations, and often has mental and emotional aspects, too. Pain signals entering the black box of the brain can be subjected further processing, and these hidden thought processes can alter the way we perceive them. We still know very little about these non-physical aspects of pain, or about the brain processes responsible for them. We do know, however, that learning and mental imagery can both diminish and enhance the experience of felt pain. Two new studies now extend these findings – one shows that subliminal learning can also alter pain responses, and the other explains how mental imagery can do so. It’s well known that simple associative learning procedures can alter responses to pain. For example, newborn babies who have diabetic mothers and are repeatedly exposed to heel pricks in the first few days of life exhibit larger pain responses during subsequent blood tests than healthy infants. Learning also appears to explain the placebo effect, and why it is often so variable. Several years ago, Karin Jensen, who is now at Harvard Medical School, and her colleagues showed that subliminal cues can reactivate consciously-learned associations to either enhance or diminish pain responses. In their latest study, the researchers set out to determine the extent to which this type of learning can occur non-consciously. © 2015 Guardian News and Media Limited

Keyword: Pain & Touch; Emotions
Link ID: 21247 - Posted: 08.01.2015

Five men with complete motor paralysis were able to voluntarily generate step-like movements thanks to a new strategy that non-invasively delivers electrical stimulation to their spinal cords, according to a new study funded in part by the National Institutes of Health. The strategy, called transcutaneous stimulation, delivers electrical current to the spinal cord by way of electrodes strategically placed on the skin of the lower back. This expands to nine the number of completely paralyzed individuals who have achieved voluntary movement while receiving spinal stimulation, though this is the first time the stimulation was delivered non-invasively. Previously it was delivered via an electrical stimulation device surgically implanted on the spinal cord. In the study, the men’s movements occurred while their legs were suspended in braces that hung from the ceiling, allowing them to move freely without resistance from gravity. Movement in this environment is not comparable to walking; nevertheless, the results signal significant progress towards the eventual goal of developing a therapy for a wide range of individuals with spinal cord injury. “These encouraging results provide continued evidence that spinal cord injury may no longer mean a life-long sentence of paralysis and support the need for more research,” said Roderic Pettigrew, Ph.D., M.D., director of the National Institute of Biomedical Imaging and Bioengineering at NIH. “The potential to offer a life-changing therapy to patients without requiring surgery would be a major advance; it could greatly expand the number of individuals who might benefit from spinal stimulation. It’s a wonderful example of the power that comes from combining advances in basic biological research with technological innovation.”

Keyword: Robotics
Link ID: 21242 - Posted: 08.01.2015

Victoria E Brings & Mark J Zylka A study finds that pain hypersensitivity in male and female mice is differentially dependent on microglia and T cells, and describes a sex-specific response to microglia-targeted pain treatments. This sex difference will be important to consider when developing treatments for pain and other neurological disorders involving microglia and immune cells. Animal studies1, 2 have spawned great interest in using microglial inhibitors such as minocycline to treat pain in humans. However, these studies were conducted largely on male rodents. Now, Sorge et al.3 have evaluated several microglial inhibitors in nerve-injured mice of both sexes. The study—led by Jeffrey Mogil, who has championed the testing of males and females in pain studies4—found that microglial inhibitors did reduce allodynia, a form of pain hypersensitivity to touch, in males. Surprisingly, however, these inhibitors were ineffective in female mice, despite a robust activation of spinal microglia (Fig. 1). The authors instead found that cells of the adaptive immune system promote pain hypersensitivity in females. Although focused on pain, these findings could have implications for other neurological disorders that disproportionately affect one sex, such as autism and neurodegeneration, and in which microglia and immune cells are implicated5, 6. Figure 1: Pain mechanisms differ in male and female mice. Pain mechanisms differ in male and female mice. Nerve injury activates microglial cells in the spinal cord of male and female mice, but microglial inhibitors only block allodynia in males. P2RX4 is upregulated in males only. Female mice have about twice as many T cells as males. Testosterone increases PPARα and decreases PPARγ gene expression in T cells. Compounds that activate PPARα inhibit mechanical pain hypersensitivity (allodynia) in males, whereas those that activate PPARγ inhibit allodynia in females. © 2015 Macmillan Publishers Limited

Keyword: Pain & Touch; Glia
Link ID: 21229 - Posted: 07.29.2015

By Annick Laurent Can you tell a pygmy blue whale from an Antarctic blue whale? If not, you aren’t alone. Marine biologists have had trouble distinguishing these enormous mammals with mottled skin patterns ever since they began studying them—and that has complicated efforts to figure out where they breed and how to best protect them. Now, researchers have caught a break thanks to a pygmy whale named Isabela. Researchers first photographed the whale and collected her DNA in 1998 in the waters off the Galapagos Islands. Then, in 2006, another team photographed and collected samples from a similar looking whale off Chile (both photos above). Now, in a study published online before print in Marine Mammal Science, scientists compared those samples and photographs, and discovered that they both belonged to the same whale. That means Isabela (named after the lead author’s daughter to represent hope for future preservation efforts) migrated a minimum of 5200 km, the longest recorded latitudinal migration made by any Southern Hemisphere blue whale on record. The findings suggest Chile's and the Galapagos’ blue whale aggregations are connected, meaning those feeding in the Gulf of Corcovado off Chile may be breeding in the Tropical Eastern Pacific. Knowing where this species migrates—including its feeding and breeding grounds—can help conservationists and governments better establish marine protected areas, the team says. © 2015 American Association for the Advancement of Science

Keyword: Animal Migration
Link ID: 21213 - Posted: 07.25.2015

By Smitha Mundasad Health reporter A type of diabetes drug may offer a glimmer of hope in the fight against Parkinson's disease, research in the journal Plos Medicine suggests. Scientists found people taking glitazone pills were less likely to develop Parkinson's than patients on other diabetes drugs. But they caution the drugs can have serious side-effects and should not be given to healthy people. Instead, they suggest the findings should prompt further research. 'Unintended benefits' There are an estimated 127,000 people in the UK with Parkinson's disease, which can lead to tremor, slow movement and stiff muscles. And charities say with no drugs yet proven to treat the condition, much more work is needed in this area. The latest study focuses solely on people with diabetes who did not have Parkinson's disease at the beginning of the project. Researchers scoured UK electronic health records to compare 44,597 people prescribed glitazone pills with 120,373 people using other anti-diabetic treatment. They matched participants to ensure their age and stage of diabetes treatment were similar. Scientists found fewer people developed Parkinson's in the glitazone group - but the drug did not have a long-lasting benefit. Any potential protection disappeared once patients switched to another type of pill. Dr Ian Douglas, lead researcher at the London School of Hygiene and Tropical Medicine, said: "We often hear about negative side-effects associated with medications, but sometimes there can also be unintended beneficial effects. "Our findings provide unique evidence that we hope will drive further investigation into potential drug treatments for Parkinson's disease." © 2015 BBC

Keyword: Parkinsons
Link ID: 21199 - Posted: 07.22.2015

Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Prions
Link ID: 21190 - Posted: 07.20.2015

By Sarah Schwartz Scientists think they have a new understanding of a potential long-lasting, targeted treatment for chronic pain. When injected into the spinal cord of a mouse with nerve damage, cells extracted from mouse bone marrow flock to injured cells and produce a pain-relieving protein, researchers report July 13 in the Journal of Clinical Investigation. The results may lead to better chronic pain treatments in humans. The specialized cells honed in on their ultimate destination by following chemical signals released by the injured nerve cells. There, the injected cells produced an anti-inflammatory protein, called transforming growth factor beta 1 (TGFB1), which provided long-term pain relief. Researchers had known that the marrow cells relieved pain, but didn’t know how, says study coauthor Ru-Rong Ji, a neurobiologist at Duke University Medical Center. “These cells make drugs at sites of injury,” says biologist Arnold Caplan of Case Western Reserve University in Cleveland. “They’re drugstores.” Ji and colleagues found that they could relieve chronic nerve pain in mice by injecting 250,000 cells or fewer into the narrow space under the spinal cord membrane. This site is protected by the blood-brain barrier, preventing immune attacks on the injected cells and allowing these cells to live longer, Ji says. Some clinical trials inject cells like these into the bloodstream, Caplan says, requiring the use of many more cells, many of which get stuck in the lungs and liver. © Society for Science & the Public 2000 - 2015

Keyword: Pain & Touch
Link ID: 21167 - Posted: 07.14.2015

Carl Zimmer A single neuron can’t do much on its own, but link billions of them together into a network and you’ve got a brain. But why stop there? In recent years, scientists have wondered what brains could do if they were linked together into even bigger networks. Miguel A. Nicolelis, director of the Center for Neuroengineering at Duke University, and his colleagues have now made the idea a bit more tangible by linking together animal brains with electrodes. In a pair of studies published on Thursday in the journal Scientific Reports, the researchers report that rats and monkeys can coordinate their brains to carry out such tasks as moving a simulated arm or recognizing simple patterns. In many of the trials, the networked animals performed better than individuals. “At least some times, more brains are better than one,” said Karen S. Rommelfanger, director of the Neuroethics Program at the Center for Ethics at Emory University, who was not involved in the study. Brain-networking research might someday allow people to join together in useful ways, Dr. Rommelfanger noted. Police officers might be able to make collective decisions on search-and-rescue missions. Surgeons might collectively operate on a single patient. But she also warned that brain networks could create a host of exotic ethical quandaries involving privacy and legal responsibility. If a brain network were to commit a crime, for example, who exactly would be guilty? © 2015 The New York Times Company

Keyword: Robotics
Link ID: 21160 - Posted: 07.11.2015

By Esther Hsieh Strap on a headset, immerse yourself in an alternate reality and cure your pain—that's the idea of a recent study in Psychological Science. Most people think of pain as something that happens in the body—I twist my head too far, and my neck sends a “pain signal” to the brain to indicate that the twisting hurts. In reality, pain is simply the brain telling us we are in danger. Although certain nerve endings throughout the body can indeed detect bodily harm, their signals are only one factor that the brain uses to determine if we should experience pain. Many cases of chronic pain are thought to be the result of obsolete brain associations between movement and pain. To explore the mind's influence over pain, Daniel Harvie, a Ph.D. candidate at the University of South Australia, and his colleagues asked 24 participants who suffer from chronic neck pain to sit in a chair while wearing virtual-reality glasses and turn their head. The displays were manipulated to make the participants think that they were turning their head more or less than they actually were. Subjects could swivel their head 6 percent more than usual if the virtual reality made them think they were turning less, and they could rotate 7 percent less than usual when they thought they were turning more. The findings suggest that virtual-reality therapy has the potential to retrain the brain to understand that once painful movements are now safe, extinguishing the association with danger. © 2015 Scientific American

Keyword: Pain & Touch
Link ID: 21155 - Posted: 07.11.2015

By JAMES GORMAN Call it the case of the homing lizards. It’s a small mystery. No one of any species is murdered. But the central question is one that has prompted plenty of scientific research: How do animals find their way home? The lizards in this case are anoles — abundant, mostly small reptiles that thrive in the Caribbean. The species is Anolis gundlachi. The lead detective is Manuel Leal, a biologist at the University of Missouri. He has been studying the behavior of anoles for more than 20 years. For about three years, Dr. Leal has been trying to understand how the anole finds its way back to its own territory after being carried into the rain forest. And as he told an audience in June at the annual meeting of the Animal Behavior Society in Anchorage, the case is far from closed. First, a bit of background. Anoles are particularly abundant in the dense vegetation of the rain forests in Puerto Rico, where Dr. Leal studies them. Each species is tied to a very specific environment. For instance, many live on tree trunks, but only a particular part of the trunk. Trunk-ground anoles live only in the space from the ground up to six feet or so. Trunk-crown anoles live above them, up to the crown of the tree. Twig anoles live way up high. Several years ago, Dr. Leal was studying competition between two species. If he removed all of the trunk-ground anoles, he wondered, would the trunk-crown lizards extend their territory farther down the tree? He ran into a problem, however. He would take the trunk-ground lizards far from their home territory to make room for their upstairs neighbors, and then release them. But in a reptilian version of the children’s song, “The Cat Came Back,” the lizards wouldn’t stay away. “Lizards kept showing up in the territory that had just been scoured for lizards,” he said. Dr. Leal wondered whether new anoles were appearing in empty territory or the old ones were returning. But how could a lizard that had never left home find its way back through 25 yards or so of dense rain forest? © 2015 The New York Times Company

Keyword: Animal Migration
Link ID: 21141 - Posted: 07.07.2015

Moheb Costandi Different immune cells regulate pain sensitization in male and female mice, according to research published on 29 June in Nature Neuroscience1. The surprising biological divide may explain why some clinical trials of pain drugs have failed, and highlights shortcomings in the way that many researchers design their experiments. The immune system has important roles in chronic pain, with cells called microglia being key players. Microglia express a protein called brain-derived neurotrophic factor (BDNF) to signal to spinal-cord neurons. When injury or inflammation occurs, this signal sensitizes the body to pain, so that even light touch hurts. Robert Sorge, a psychologist at the University of Alabama in Birmingham, and his colleagues induced persistent pain and inflammation in healthy male and female mice by severing two of the three sciatic nerve branches in their hind paws. Seven days later, they injected the animals with one of three drugs that inhibit microglial function. They found that all three drugs reversed pain sensitization in the male animals, as had been previously reported. But the treatments had no effect on the females, even though the animals had displayed equivalent levels of pain. The researchers also genetically engineered mice in which the BDNF gene could be deleted in microglia at any time during the animals' lives. At first, these animals exhibited normal responses to a nerve injury. Killing the microglia one week later extinguished that hypersensitivity in the male animals, but not in the females. This confirmed that in males, hypersensitivity to pain depends on BDNF signals from microglia, but that in females it is mediated by some other mechanism. © 2015 Nature Publishing Group,

Keyword: Pain & Touch; Sexual Behavior
Link ID: 21113 - Posted: 06.30.2015