Chapter 5. The Sensorimotor System

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By NICHOLAS BAKALAR Chronic pain may be linked to an increasing risk for dementia. Researchers interviewed 10,065 people over 62 in 1998 and 2000, asking whether they suffered “persistent pain,” defined as being often troubled with moderate or severe pain. Then they tracked their health through 2012. After adjusting for many variables, they found that compared with those who reported no pain problems, people who reported persistent pain in both 1998 and 2000 had a 9 percent more rapid decline in memory performance. Moreover, the probability of dementia increased 7.7 percent faster in those with persistent pain compared with those without. The study, in JAMA Internal Medicine, does not prove cause and effect. But chronic pain may divert attention from other mental activity, leading to poor memory, and some studies have found that allaying pain with opioids can lead to cognitive improvements. Still, the lead author, Dr. Elizabeth L. Whitlock, an anesthesiologist at the University of California at San Francisco, acknowledged that treatment with opioids is problematic, and that safely controlling chronic pain is a problem that so far has no satisfactory solution. “I’d encourage clinicians to be aware of the cognitive implications of a simple report of pain,” she said. “It’s a simple question to ask, and the answer can be used to identify a population at high risk of functional and cognitive problems.” © 2017 The New York Times Company

Keyword: Alzheimers; Pain & Touch
Link ID: 23719 - Posted: 06.08.2017

By Nicholette Zeliadt, For 6-year-old Macey, lunchtime at school is not so much a break from reading and math as it is an hour rife with frustration. Here’s how Macey’s mother, Victoria, describes Macey’s typical lunch break: In her special-education classroom an hour north of San Francisco, Macey’s classmates gather at a big square table, chattering away and snatching one another’s food. Macey, meanwhile, is sequestered away at a small white table in a corner, facing a bookshelf. She grabs the handle of a spoon using the palm of her right hand, awkwardly scoops up rice and spills it onto her lap. She wants to be at the big table with her peers, but she sits with an aide away from the other children to minimize distractions while she eats. (Victoria requested that we use her and Macey’s first names only, to protect their privacy.) After lunch, the children spill out onto the playground. Macey, wearing a helmet, trails behind, holding her aide’s hand. She can walk, but she often trips on uneven surfaces and falls over. She tends to misjudge heights, and once pulled a muscle while climbing on playground equipment. When she was 3, she tripped and fell headfirst out of a sandbox, scraping her face, chipping one tooth and dislodging another. Macey has little trouble moving around the house because it has few stairs and her mother never changes the layout of the rooms. Victoria’s biggest concern is that Macey’s movement troubles interfere with her social life. © 2017 Scientific American,

Keyword: Autism; Movement Disorders
Link ID: 23713 - Posted: 06.06.2017

Mo Costandi Since 1997, more than 100,000 Parkinson’s Disease patients have been treated with deep brain stimulation (DBS), a surgical technique that involves the implantation of ultra-thin wire electrodes. The implanted device, sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a structure called the subthalamic nucleus, located near the centre of the brain, and effectively alleviates many of the physical symptoms of the disease, such as tremor, muscle rigidity, and slowed movements. DBS is generally safe but, like any surgical procedure, comes with some risks. First and foremost, it is highly invasive, requiring small holes to be drilled in the patient’s skull, through which the electrodes are inserted. Potential complications of this include infection, stroke, and bleeding on the brain. The electrodes, which are implanted for long periods of time, sometimes move out of place; they can also cause swelling at the implantation site; and the wire connecting them to the battery, typically placed under the skin of the chest, can erode, all of which require additional surgical procedures. Now, researchers at the Massachusetts Institute of Technology have a developed a new method that can stimulate cells deep inside the brain non-invasively, using multiple electric fields applied from outside the organ. In a study published today in the journal Neuron, they show that the method can selectively stimulate deep brain structures in live mice, without affecting the activity of cells in the overlying regions, and also that it can be easily adjusted to evoke movements by stimulation of the motor cortex. © 2017 Guardian News and Media Limited o

Keyword: Parkinsons
Link ID: 23700 - Posted: 06.02.2017

By Matthew Hutson The life of a sheep is not as cushy as it looks. They suffer injury and infection, and can’t tell their human handlers when they’re in pain. Recently, veterinarians have developed a protocol for estimating the pain a sheep is in from its facial expressions, but humans apply it inconsistently, and manual ratings are time-consuming. Computer scientists at the University of Cambridge in the United Kingdom have stepped in to automate the task. They started by listing several “facial action units” (AUs) associated with different levels of pain, drawing on the Sheep Pain Facial Expression Scale. They manually labeled these AUs—nostril deformation, rotation of each ear, and narrowing of each eye—in 480 photos of sheep. Then they trained a machine-learning algorithm by feeding it 90% of the photos and their labels, and tested the algorithm on the remaining 10%. The program’s average accuracy at identifying the AUs was 67%, about as accurate as the average human, the researchers will report today at the IEEE International Conference on Automatic Face and Gesture Recognition in Washington, D.C. Ears were the most telling cue. Refining the training procedure further boosted accuracy. Given additional labeled images, the scientists expect their method would also work with other animals. Better diagnosis of pain could lead to quicker treatment. © 2017 American Association for the Advancement of Science. A

Keyword: Pain & Touch
Link ID: 23694 - Posted: 06.02.2017

By Bob Grant Prosthetic limbs are rejected by amputees’ bodies at a rate of about 20 percent. Researchers at MIT are seeking to reduce that number, using an amputation procedure that encourages increased feedback between muscles, tendons, and the nervous system so that an artificial limb might stimulate them in a more natural way—giving patients a better sense of proprioception, or where their limb is in space. The key to the surgical technique, demonstrated in rats so far, is to emulate the normal agonist-antagonist pairing of muscles (think biceps and triceps) at the amputation site so that the muscles and nerves surrounding a prosthetic can sense and transmit proprioceptive information about the artificial limb and how much force is being applied to it. The researchers published their work today (May 31) in Science Robotics. “We’re talking about a dramatic improvement in patient care,” Hugh Herr, an MIT professor of media arts and sciences and a coauthor of the study, said in a statement. “Right now there’s no robust neural method for a person with limb amputation to feel proprioceptive positions and forces applied to the prosthesis. Imagine how that would completely hinder one’s ability to move, to successfully balance, or to manipulate objects.” Herr, himself a double-amputee, and his team operated on seven rats, cutting through muscles and nerves in their hind legs. The researchers then grafted on paired muscles, wiring them up to severed nerves. After healing for four months, the rats’ new muscles were contracting and relaxing in tandem, as in naturally paired muscles, and sending electrical signals that reflected the amplitude of the artificial stimulation Herr and his colleagues applied. © 1986-2017 The Scientist

Keyword: Movement Disorders
Link ID: 23693 - Posted: 06.02.2017

Laurel Hamers Last year, Joan Peay slipped on her garage steps and smashed her knee on the welcome mat. Peay, 77, is no stranger to pain. The Tennessee retiree has had 17 surgeries in the last 35 years — knee replacements, hip replacements, back surgery. She even survived a 2012 fungal meningitis outbreak that sickened her and hundreds of others, and killed 64. This knee injury, though, “hurt like the dickens.” When she asked her longtime doctor for something stronger than ibuprofen to manage the pain, he treated her like a criminal, Peay says. His response was frustrating: “He’s known me for nine years, and I’ve never asked him for pain medicine other than what’s needed after surgery,” she says. She received nothing stronger than over-the-counter remedies. A year after the fall, she still lives in constant pain. Just five years ago, Peay might have been handed a bottle of opioid painkillers for her knee. After all, opioids — including codeine, morphine and oxycodone — are some of the most powerful tools available to stop pain. Hitting opioid receptors in the peripheral nervous system keeps pain messages from reaching the brain. But opioids can cause problems by overstimulating the brain’s reward system and binding to receptors in the brain stem and gut. But an opioid addiction epidemic spreading across the United States has soured some doctors on the drugs. Many are justifiably concerned that patients will get hooked or share their pain pills with friends and family. And even short-term users risk dangerous side effects: The drugs slow breathing and can cause constipation, nausea and vomiting. |© Society for Science & the Public 2000 - 2017

Keyword: Pain & Touch; Drug Abuse
Link ID: 23686 - Posted: 05.31.2017

By JANE E. BRODY A neighbor of mine was recently told he has a devastating neurological disorder that is usually fatal within a few years of diagnosis. Though a new drug was recently approved for the illness, treatments may only slow progression of the disease for a time or extend life for maybe two or three months. He is a man of about 60 I’ve long considered the quintessential Mr. Fix-it, able to repair everything from bicycles to bathtubs. Now he is facing amyotrophic lateral sclerosis, or Lou Gehrig’s disease — a disease that no one yet knows how to fix. I can only imagine what he is going through because he does not want to talk about it. However, many others similarly afflicted have openly addressed the challenges they faced, though it is usually up to friends and family to express them and advocate for more and better research and public understanding. A.L.S. attacks the nerve cells in the brain and spinal cord that control voluntary muscle movements, like chewing, walking, breathing, swallowing and talking. It is invariably progressive. Lacking nervous system stimulation, the muscles soon begin to weaken, twitch and waste away until individuals can no longer speak, eat, move or even breathe on their own. Last year, the Centers for Disease Control and Prevention estimated that between 14,000 and 15,000 Americans have A.L.S., which makes it sound like a rare disease, but only because life expectancy is so short. A.L.S. occurs throughout the world, and it is probably far more common than generally thought. Over the course of a lifetime, one person in about 400 is likely to develop it, a risk not unlike that of multiple sclerosis. But with the rare exception of an outlier like the brilliant physicist Stephen Hawking, who has had A.L.S. for more than 50 years, it usually kills so quickly that many people do not know anyone living with this disease. Only one person in 10 with A.L.S. is likely to live for a decade or longer. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23675 - Posted: 05.29.2017

Patients who are told their medication can have certain side-effects may report these symptoms more often than patients who aren't aware their treatment carries these risks, a study of popular cholesterol pills suggests. Researchers focused on what they dubbed the "nocebo" effect, or the potential for people to complain of treatment-related side-effects when they think they're taking a specific drug but are actually given a placebo, or dummy pill, without any active ingredients. "It has been recognized for many years that when patients are warned about possible adverse reactions to a drug, they are much more likely to complain of these side effects than when they are unaware of the possibility that such side-effects might occur," said senior study author Dr. Peter Sever, a researcher at Imperial College London. To test this "nocebo" effect, researchers first randomly assigned about 10,000 trial participants in the UK, Ireland and Scandinavia to take either a statin pill to lower cholesterol or a placebo, then followed people for around three years to see how often they complained of four known statin side-effects: Patients on statins and on placebo pills reported similar rates of muscle aches and erectile dysfunction, the study found. People taking placebo also reported higher rates of sleep difficulties than patients on statins. ©2017 CBC/Radio-Canada.

Keyword: Pain & Touch
Link ID: 23665 - Posted: 05.27.2017

Susan Milius A question flamingo researchers get asked all the time — why the birds stand on one leg — may need rethinking. The bigger puzzle may be why flamingos bother standing on two. Balance aids built into the birds’ basic anatomy allow for a one-legged stance that demands little muscular effort, tests find. This stance is so exquisitely stable that a bird sways less to keep itself upright when it appears to be dozing than when it’s alert with eyes open, two Atlanta neuromechanists report May 24 in Biology Letters. “Most of us aren’t aware that we’re moving around all the time,” says Lena Ting of Emory University, who measures what’s called postural sway in standing people as well as in animals. Just keeping the human body vertical demands constant sensing and muscular correction for wavering. Even standing robots “are expending quite a bit of energy,” she says. That could have been the case for flamingos, she points out, since effort isn’t always visible. Translate that improbably long flamingo leg into human terms, and the visible part of the leg would be just the shin down. A flamingo’s hip and knee lie inside the bird’s body. Ting and Young-Hui Chang of the Georgia Institute of Technology tested balance in fluffy young Chilean flamingos coaxed onto a platform attached to an instrument that measures how much they sway. Keepers at Zoo Atlanta hand-rearing the test subjects let researchers visit after feeding time in hopes of catching youngsters inclined toward a nap — on one leg on a machine. “Patience,” Ting says, was the key to any success in this experiment. |© Society for Science & the Public 2000 - 2017

Keyword: Sleep
Link ID: 23656 - Posted: 05.24.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

Laura Beil Even though a sprained ankle rarely needs an opioid, a new study of emergency room patients found that about 7 percent of patients got sent home with a prescription for the potentially addictive painkiller anyway. And the more pills prescribed, the greater the chance the prescription would be refilled, raising concerns about continued use. The research adds to evidence that it’s hard for some people to stop taking the pills even after a brief use. State officials in New Jersey recently enacted a law limiting first-time prescriptions to a five-day supply, and other states should consider similar restrictions, says Kit Delgado, an assistant professor of Emergency Medicine and Epidemiology at the University of Pennsylvania. “The bottom line is that we need to do our best not to expose people to opioids,” Delgado says. “And if we do, start with the smallest quantity possible.” The research was presented May 17 at the Society for Academic Emergency Medicine’s annual meeting in Orlando. Previous research has found that the more opioids such as hydrocodone and oxycodone are prescribed, the more likely patients are to keep taking them. But previous studies have been too broad to account for differences in diagnoses — for instance, whether people who received refills kept taking the drug simply because they still were in pain, Delgado says. He and colleagues limited their study to prescriptions written after ankle sprains to people who had not used an opioid in the previous six months. Usually, those injuries aren’t serious and don’t require opioids. |© Society for Science & the Public 2000 - 2017

Keyword: Drug Abuse; Pain & Touch
Link ID: 23638 - Posted: 05.20.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

Keyword: Parkinsons
Link ID: 23636 - Posted: 05.19.2017

By Roman Liepelt and Jack Brooks An amputee struggles to use his new prosthetic limb. A patient with a frontal-lobe brain lesion insists that her left hand has a mind of its own. The alleged criminal claims in court that he did not fire the gun, even though several eyewitnesses watched him do it. Each of these individuals is grappling with two elements of the mind-body connection: ownership, or an ability to separate ourselves from the physical and social environments, and agency, a conviction that we have control over our limbs. We are quick to investigate a sticker placed on our forehead when looking in a mirror, recognizing the foreign object as abnormal. The human brain typically handles these phenomena by comparing neural signals encoding the intended action with those signals carrying sensory feedback. When we are born, we make erratic reaching and kicking movements to map our body and to calibrate our sensorimotor system. During infancy, these movements solidify our self-awareness, and around the time we first walk, we are quick to investigate a sticker placed on our forehead when looking in a mirror, recognizing the foreign object as abnormal. By the age of four, our brains are proficient at distinguishing self and other. In the amputee, the brain lesion patient, and the defendant on trial, the sense of self is disrupted due to discordance between sensory feedback from the limb and the brain’s expectations of how a movement should feel. © 1986-2017 The Scientist

Keyword: Pain & Touch
Link ID: 23625 - Posted: 05.17.2017

By DENISE GRADY A new drug for amyotrophic lateral sclerosis, or Lou Gehrig’s disease, was approved on Friday by the Food and Drug Administration. The drug, called Radicava or edaravone, slowed the progression of the degenerative disease in a six-month study in Japan. It must be given by intravenous infusion and will cost $145,524 a year, according to its manufacturer, MT Pharma America, a subsidiary of the Japanese company Mitsubishi Tanabe Pharma Corporation. Radicava is only the second drug ever approved to treat A.L.S. The first, riluzole, was approved by the F.D.A. more than 20 years ago. Riluzole can increase survival by two or three months. There is no information yet about whether Radicava has any effect on survival. In the study in Japan, 137 patients were picked at random to receive either Radicava or a placebo. At the end of six months, the condition of those taking the drug declined less than those receiving placebos. Dr. Neil A. Shneider, director of the Eleanor and Lou Gehrig ALS Center at Columbia University Medical Center, said, “The effect is modest but significant.” He added, “I’m very happy, frankly, that there is a second drug approved for A.L.S.” The disease kills nerve cells that control voluntary muscles, so patients gradually weaken and become paralyzed. Most die within three to five years, usually from respiratory failure. About 12,000 to 15,000 people in the United States have A.L.S., according to the Centers for Disease Control and Prevention. Dr. Shneider predicted that patients would be eager to try the new drug. He said several of his patients were already receiving it because they had obtained it themselves from Japan. If more want it, he will prescribe it, he said. “It’s very safe,” he said. But he was uncertain about whether he would actually recommend it, because the method of administration is difficult. Patients have to have an intravenous line inserted and left in place indefinitely, which poses an infection risk. The first round of treatment requires a one-hour infusion every day for 14 days, followed by 14 days off. After that, the infusions are given daily for 10 out of 14 days, with 14 days off. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Trophic Factors
Link ID: 23585 - Posted: 05.06.2017

By Moheb Costandi Pain in infants is heartbreaking for new parents, and extremely difficult to treat effectively—if at all. Every year an estimated 15 million babies are born prematurely, most of whom will then undergo numerous lifesaving but painful procedures, such as heel pricking or insertion of a thin tube known as a cannula to deliver fluids or medicine. Preterm babies in the intensive care unit are subjected to an average of 11 such “skin-breaking” procedures per day, but analgesia is only used just over one third of the time. We know that repetitive, painful procedures in early infancy can impact brain development negatively—so why is pain in infants so undertreated? One reason is the lack of standard guidelines for administering the drugs. Some analgesics given to adults are unsuitable for infants, and those that can be used often have different effects in children, making dosing a problem. What is more, newborn babies are incapable of telling us how they feel, making it impossible to determine how effective any painkiller might be. Researchers at the University of Oxford may now have overcome this latter challenge, however. They report May 3 in Science Translational Medicine having identified a pain-related brain wave signal that responds to analgesics, and could be used to measure the drugs’ efficacy. Until as recently as the 1980s, it was assumed that newborn babies do not feel pain, and that giving them analgesics would do more harm than good. Although these misconceptions have been cleared up, we still have very little understanding of infant pain, and so treating it is a huge challenge for clinicians. © 2017 Scientific American

Keyword: Pain & Touch
Link ID: 23576 - Posted: 05.05.2017

Douglas Fox Six times a day, Katrin pauses whatever she's doing, removes a small magnet from her pocket and touches it to a raised patch of skin just below her collar bone. For 60 seconds, she feels a soft vibration in her throat. Her voice quavers if she talks. Then, the sensation subsides. The magnet switches on an implanted device that emits a series of electrical pulses — each about a milliamp, similar to the current drawn by a typical hearing aid. These pulses stimulate her vagus nerve, a tract of fibres that runs down the neck from the brainstem to several major organs, including the heart and gut. The technique, called vagus-nerve stimulation, has been used since the 1990s to treat epilepsy, and since the early 2000s to treat depression. But Katrin, a 70-year-old fitness instructor in Amsterdam, who asked that her name be changed for this story, uses it to control rheumatoid arthritis, an autoimmune disorder that results in the destruction of cartilage around joints and other tissues. A clinical trial in which she enrolled five years ago is the first of its kind in humans, and it represents the culmination of two decades of research looking into the connection between the nervous and immune systems. For Kevin Tracey, a neurosurgeon at the Feinstein Institute for Medical Research in Manhasset, New York, the vagus nerve is a major component of that connection, and he says that electrical stimulation could represent a better way to treat autoimmune diseases, such as lupus, Crohn's disease and more. Several pharmaceutical companies are investing in 'electroceuticals' — devices that can modulate nerves — to treat cardiovascular and metabolic diseases. But Tracey's goal of controlling inflammation with such a device would represent a major leap forward, if it succeeds. © 2017 Macmillan Publishers Limited

Keyword: Neuroimmunology; Pain & Touch
Link ID: 23573 - Posted: 05.04.2017

Laura Sanders An electrode on top of a newborn’s scalp, near the soft spot, can measure when the baby feels pain. The method, described online May 3 in Science Translational Medicine, isn’t foolproof, but it brings scientists closer to being able to tell when infants are in distress. Pain assessment in babies is both difficult and extremely important for the same reason: Babies don’t talk. That makes it hard to tell when they are in pain, and it also means that their pain can be more easily overlooked, says Carlo Bellieni, a pediatric pain researcher at the University Hospital Siena in Italy. Doctors rely on a combination of clues such as crying, wiggling and facial grimacing to guess whether a baby is hurting. But these clues can mislead. “Similar behaviors occur when infants are not in pain, for example if they are hungry or want a cuddle,” says study coauthor Rebeccah Slater of the University of Oxford. By relying on brain activity, the new method promises to be a more objective measurement. Slater and colleagues measured brain activity in 18 newborns between 2 and 5 days old. Electroencephalography (EEG) recordings from electrodes on the scalp picked up collective nerve cell activity as babies received a heel lance to draw blood or a low-intensity bop on the foot, a touch that’s a bit like being gently poked with a blunt pencil. One electrode in particular, called the Cz electrode and perched on the top of the head, detected a telltale neural spike between 400 and 700 milliseconds after the painful event. This brain response wasn’t observed when these same babies received a sham heel lance or an innocuous touch on the heel. |© Society for Science & the Public 2000 - 2017

Keyword: Pain & Touch; Development of the Brain
Link ID: 23566 - Posted: 05.04.2017

Amber Dance Biologist Leo Smith held an unusual job while an undergraduate student in San Diego. Twice a year, he tagged along on a chartered boat with elderly passengers. The group needed him to identify two particular species of rockfish, the chilipepper rockfish and the California shortspine thornyhead. Once he’d found the red-orange creatures, the passengers would stab themselves in the arms with the fishes’ spines. Doing so, the seniors believed, would relieve their aching arthritic joints. Smith, now at the University of Kansas in Lawrence, didn’t think much of the practice at the time, but now he wonders if those passengers were on to something. Though there’s no evidence that anything in rockfish venom can alleviate pain — most fish stings are, in fact, quite painful themselves — some scientists suspect fish venom is worth a look. Studying the way venom molecules from diverse fishes inflict pain might help researchers understand how nerve cells sense pain and lead to novel ways to dull the sensation. Smith is one of a handful of scientists who are studying fish venoms, and there’s plenty to investigate. An estimated 7 to 9 percent of fishes, close to 3,000 species, are venomous, Smith’s work suggests. Venomous fishes are found in freshwater and saltwater, including some stingrays, catfishes and stonefishes. Some, such as certain fang blennies, are favorites in home aquariums. Yet stinging fishes haven’t gotten the same attention from scientists as snakes and other venomous creatures. |© Society for Science & the Public 2000 - 2017

Keyword: Pain & Touch; Neurotoxins
Link ID: 23515 - Posted: 04.20.2017

Laurel Hamers Earth’s magnetic field helps eels go with the flow. The Gulf Stream fast-tracks young European eels from their birthplace in the Sargasso Sea to the European rivers where they grow up. Eels can sense changes in Earth’s magnetic field to find those highways in a featureless expanse of ocean — even if it means swimming away from their ultimate destination at first, researchers report in the April 13 Current Biology. European eels (Anguilla anguilla) mate and lay eggs in the salty waters of the Sargasso Sea, a seaweed-rich region in the North Atlantic Ocean. But the fish spend most of their adult lives living in freshwater rivers and estuaries in Europe and North Africa. Exactly how eels make their journey from seawater to freshwater has baffled scientists for more than a century, says Nathan Putman, a biologist with the National Oceanic and Atmospheric Administration in Miami. The critters are hard to track. “They’re elusive,” says study coauthor Lewis Naisbett-Jones, a biologist now at the University of North Carolina at Chapel Hill. “They migrate at night and at depth. The only reason we know they spawn in the Sargasso Sea is because that’s where the smallest larvae have been collected.” |© Society for Science & the Public 2000 - 2017.

Keyword: Animal Migration
Link ID: 23492 - Posted: 04.14.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23488 - Posted: 04.14.2017