Chapter 5. The Sensorimotor System

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.

Links 1 - 20 of 2842

Ian Sample Science editor Rats with spinal cord injuries have regained the use of their paws after being given a groundbreaking gene therapy that helps to mend damaged nerves in the spine. The new therapy works by dissolving the dense scar tissue that forms a thick barrier between severed nerves when the spinal column is broken. Animals that were given the treatment produced an enzyme called chondroitinase which breaks down scar tissue and allows the broken nerves to reconnect with each other. Tests showed that when the therapy was given for two months, rats relearned the kinds of skilled movements they needed to grab little sugar balls from a platform. “The gene therapy has enabled us to treat large areas of the spinal cord with only one injection,” said Elizabeth Bradbury, who led the research at King’s College London. “This is important because the spinal cord is long and the pathology spreads down its whole length after injury.” While more animal studies are needed before the therapy can go into human trials, researchers hope that ultimately the treatment will help people with spinal injuries who have lost the ability to perform daily tasks, such as using a knife and fork, picking up a mug, and writing. © 2018 Guardian News and Media Limited

Keyword: Regeneration
Link ID: 25095 - Posted: 06.16.2018

Christine Herman A painkiller prescription could become a ticket for medical marijuana in Illinois. Lawmakers there passed a bill making anyone with a prescription for opioids eligible for its medical cannabis program. With this move, Illinois joins a growing number of states turning to legal cannabis in the fight against painkiller addiction. "As we see the horrible damage inflicted by opioid use and misuse, it seems like a very low-cost and low-risk alternative," says state Sen. Don Harmon, a Democrat from Oak Park, Ill., and sponsor of the Senate version of the bill. The Alternatives to Opioids Act would allow millions of patients to apply for temporary access to the state's existing medical cannabis pilot program. The bill, which passed on May 31, is now awaiting Republican Gov. Bruce Rauner's signature. Though the bill has bipartisan support, marijuana advocates have some doubts about whether he'll sign it, given his past opposition to medical cannabis. Lawmakers in several states have taken action to initiate or expand their medical marijuana programs in light of the opioid crisis. Among them, in Georgia Gov. Nathan Deal signed a law adding PTSD and intractable pain to the list of conditions covered in its medical marijuana program in May. And New York state Sen. George Amedore, a Republican, introduced legislation that would allow doctors to prescribe cannabis oil as an alternative to opioids for certain conditions. Under Illinois' proposed new law, anyone 21 or older with a condition for which opioids might be prescribed could get near-immediate access to cannabis products at licensed dispensaries by presenting paperwork signed by their doctor. They would no longer be fingerprinted or need criminal background checks, or wait months for approval. The measure would reduce the backlog of applications, Harmon says. © 2018 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 25094 - Posted: 06.16.2018

By James Gallagher Health and science correspondent, BBC News Scientists say they have taken a significant step towards the goal of giving paralysed people control of their hands again. The team at King's College London used gene therapy to repair damage in the spinal cord of rats. The animals could then pick up and eat sugar cubes with their front paws. It is early stage research, but experts said it was some of the most compelling evidence that people's hand function could one day be restored. The spinal cord is a dense tube of nerves carrying instructions from the brain to the rest of the body. The body repairs a wounded spinal cord with scar tissue. However, the scar acts like a barrier to new connections forming between nerves. How the gene therapy works The researchers were trying to dissolve components of the scar tissue in the rats' spinal cord. They needed to give cells in the cord a new set of genetic instructions - a gene - for breaking down the scar. The instructions they gave were for an enzyme called chondroitinase. And they used a virus to deliver them. Finally, a drug was used to activate the instructions. The animals regained use of their front paws after the gene therapy had been switched on for two months. Dr Emily Burnside, one of the researchers, said: "The rats were able to accurately reach and grasp sugar pellets. "We also found a dramatic increase in activity in the spinal cord of the rats, suggesting that new connections had been made in the networks of nerve cells." The researchers hope their approach will work for people injured in car crashes or falls. © 2018 BBC.

Keyword: Regeneration
Link ID: 25092 - Posted: 06.15.2018

by Cleve R. Wootson Jr. Kailyn Griffin, 5, experienced temporary paralysis following a tick bite in Grenada, Miss., discovered on June 6. (WLBT) As soon as Kailyn Griffin's feet hit the floor Wednesday morning, she collapsed in a heap. The 5-year-old kept trying to stand but fell every time. She was also struggling to speak, said her mother, Jessica Griffin. Her daughter had been fine when the family went out to a T-ball game the night before, NBC-affiliate WLBT in Jackson, Miss., reported. Maybe Kailyn was having a hard time waking up Wednesday morning, or perhaps her legs were asleep. Then Griffin saw the tick. She had gathered Kailyn's hair to put it in a ponytail when she spotted the arachnid, embedded in the girl's scalp, swelled with the girl's blood. She pulled the tick out and placed it in a plastic bag, then rushed to the hospital with Kailyn, WTXL reported. Doctors told Griffin it was an uncommon condition called tick paralysis. “After tons of bloodwork and a CT of the head UMMC has ruled it as tick paralysis! PLEASE for the love of god check your kids for ticks! It’s more common in children than it is adults!” Griffin, of Grenada, Miss., wrote in a Facebook post Wednesday that seemed a mixture of worry and relief. “Scary is a UNDERSTATEMENT!” Griffin could not be immediately reached for comment. It was unclear where or when she thought her daughter had acquired the tick, or how long it had been on her body. Ticks are most active from April through September, The Washington Post has reported. Tick paralysis is caused by female ticks on the verge of laying eggs. After the tick eats a blood meal and is engorged, it secretes a neurotoxin into the host, according to the American Lyme disease Foundation. The symptoms can occur five to seven days after the tick starts feeding. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 25081 - Posted: 06.12.2018

Leah Rosenbaum Migraines have plagued humans since time immemorial. Now a new migraine prevention treatment, recently approved by the U.S. Food and Drug Administration, promises long-awaited relief from the debilitating condition. But whether the drug will turn out to be a real solution for the 1 in 7 Americans who suffer from migraines, severe headaches that often come with nausea and visual auras, isn’t yet clear. Here’s what we know, and don’t know, about the new therapy. How does the drug work in the body? The new drug, Aimovig, generically called erenumab, is a type of monoclonal antibody treatment, a class of medications that resemble the antibodies that the body naturally produces to bind to infectious pathogens. These treatments work by using specially designed antibodies to target specific proteins and their receptors that contribute to disease. Aimovig, released by pharmaceutical companies Amgen Inc. and Novartis, targets the receptor for a protein called calcitonin gene-related peptide, or CGRP, that is increased in people suffering a migraine attack. The protein is released from nerve endings throughout the body, including in the meninges, the membranes that surround the brain. When it attaches to the receptor, CGRP widens blood vessels and can contribute to inflammation and pain transmission. Aimovig, delivered once a month with an EpiPen-like injector, works by blocking the receptor for CGRP, reducing pain. Blocking the protein’s receptor is kind of like putting gum in a lock, says Elizabeth Loder, a neurologist at Brigham and Women’s Hospital in Boston and at Harvard Medical School. The CGRP protein “key” is still floating around, but it can’t become activated. |© Society for Science & the Public 2000 - 2018

Keyword: Pain & Touch
Link ID: 25064 - Posted: 06.07.2018

By Ingfei Chen Each year, according to the U.S. Department of Agriculture, roughly 820,800 guinea pigs, dogs, cats, and other animals covered by the Animal Welfare Act are used in research in the U.S.; of those, about 71,370 are subjected to unalleviated pain. These stats don’t track the millions of mice and rats that are used in lab experiments and excluded from the animal protection law (although the rodents are covered by other federal regulations). Scientists and their institutions say they’re committed to keeping pain or distress to a minimum in lab animals where they can. But how do you know how much pain a mouse or a zebrafish feels? And who decides how much pain is too much? “We know if they’re in really bad pain, as much as they want a nice nest, they’re not gonna put the work into doing that.” The issue of animal suffering was in the headlines earlier this year, when landlocked Switzerland banned the culinary practice of boiling lobsters alive. No one knows for sure whether these big-clawed crustaceans, equipped with only a rudimentary nervous system, experience pain. Nonetheless, Swiss authorities now require stunning lobsters in a humane way before tossing them into the pot. I read of this milestone in crustacean rights with bemused fascination and anthropomorphic cringing, as I imagined the lobster’s hypothetical plight. But the Swiss move also made me wonder how scientists measure and deal with animal pain in research studies. Experiments that use critters to simulate human illness or injury are stepping stones to the medical treatments we all use. Yet, the benefits we reap must outweigh the costs to animal welfare for those sacrifices to be justified, ethicists and animal advocates say. Copyright 2018 Undark

Keyword: Animal Rights; Pain & Touch
Link ID: 25061 - Posted: 06.06.2018

By Ruth Williams Four patients with chronic spinal damage and a complete loss of motor and sensory functions below their waists have received transplants of human neural stem cells in a first-of-its-kind clinical trial. A report in Cell Stem Cell today (June 1) documents the procedure and the subsequent clinical follow up of the patients, who exhibit no signs of untoward effects but rather tiny hints of improvement. “It’s an extremely interesting and important piece of work,” says neurologist Eva Feldman of the University of Michigan who was not involved with the work. “The rodent model results were very compelling and . . . laid the groundwork for this very small, proof-of-concept safety trial.” While these results seem tantalizing, “the numbers [of patients] are extremely small,” says Feldman, and “the patients themselves notice no change in function or quality of life.” Severe spinal injuries can have devastating consequences, often leaving patients with complete paralysis below the injury site and with little hope of recovery. While there is currently no therapy that can promote neuronal repair in such patients, evidence from animal studies, including those carried out in primates, has indicated that transplantation of human-derived neural stem cells to the site of injury can promote some functional recovery of downstream musculature. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 25059 - Posted: 06.05.2018

By Robert F. Service Prosthetics may soon take on a whole new feel. That’s because researchers have created a new type of artificial nerve that can sense touch, process information, and communicate with other nerves much like those in our own bodies do. Future versions could add sensors to track changes in texture, position, and different types of pressure, leading to potentially dramatic improvements in how people with artificial limbs—and someday robots—sense and interact with their environments. “It’s a pretty nice advance,” says Robert Shepherd, an organic electronics expert at Cornell University. Not only are the soft, flexible, organic materials used to make the artificial nerve ideal for integrating with pliable human tissue, but they are also relatively cheap to manufacture in large arrays, Shepherd says. Modern prosthetics are already impressive: Some allow amputees to control arm movement with just their thoughts; others have pressure sensors in the fingertips that help wearers control their grip without the need to constantly monitor progress with their eyes. But our natural sense of touch is far more complex, integrating thousands of sensors that track different types of pressure, such as soft and forceful touch, along with the ability to sense heat and changes in position. This vast amount of information is ferried by a network that passes signals through local clusters of nerves to the spinal cord and ultimately the brain. Only when the signals combine to become strong enough do they make it up the next link in the chain. © 2018 American Association for the Advancement of Science.

Keyword: Robotics; Pain & Touch
Link ID: 25048 - Posted: 06.01.2018

Imagine having superhuman hearing. You’re at a noisy, cocktail party and yet your ears can detect normally inaudible sounds made by your friends’ muscles as they lean in to dish the latest gossip. But, unlike normal hearing, each of these sounds causes your ears to react in the same way. There is no difference between the quietest and loudest movements. To your superhuman ears, they all sound loud, like honking horns. According to a study funded by the National Institutes of Health, that may be how a shark’s electrosensing organ reacts when it detects teensy, tiny electrical fields emanating from nearby prey. “Sharks have this incredible ability to pick up nanoscopic currents while swimming through a blizzard of electric noise. Our results suggest that a shark’s electrosensing organ is tuned to react to any of these changes in a sudden, all-or-none manner, as if to say, ‘attack now,’” said David Julius, Ph.D., professor and chair of physiology at the University of California, San Francisco and senior author of the study published in Nature. His team studies the cells and molecules behind pain and other sensations. For instance, their results have helped scientists understand why chili peppers feel hot and menthol cool. Led by post-docs Nicholas W. Bellono, Ph.D. and Duncan B. Leitch, Ph.D., Dr. Julius’ team showed that the shark’s responses may be very different from the way the same organ reacts in skates, the flat, winged, evolutionary cousins of sharks and sting rays, and this may help explain why sharks appear to use electric fields strictly to locate prey while skates use them to find food, friends, and mates. They also showed how genes that encode for proteins called ion channels may control the shark’s unique “sixth sense.”

Keyword: Aggression; Pain & Touch
Link ID: 25038 - Posted: 05.31.2018

Deep brain stimulation has been used to treat Parkinson’s disease symptoms for 25 years, but limitations have led researchers to look for ways to improve the technique. This study describes the first fully implanted DBS system that uses feedback from the brain itself to fine-tune its signaling. The study was supported by the National Institutes of Health’s Brain Research through Advancing Innovative Technologies (BRAIN) Initiative and the National Institute of Neurological Disorders and Stroke (NINDS). “The novel approach taken in this small-scale feasibility study may be an important first step in developing a more refined or personalized way for doctors to reduce the problems patients with Parkinson’s disease face every day,” said Nick B. Langhals, Ph.D., program director at NINDS and team lead for the BRAIN Initiative. Deep brain stimulation is a method of managing Parkinson’s disease symptoms by surgically implanting an electrode, a thin wire, into the brain. Traditional deep brain stimulation delivers constant stimulation to a part of the brain called the basal ganglia to help treat the symptoms of Parkinson’s. However, this approach can lead to unwanted side effects, requiring reprogramming by a trained clinician. The new method described in this study is adaptive, so that the stimulation delivered is responsive in real time to signals received from the patient’s brain. “This is the first time a fully implanted device has been used for closed-loop, adaptive deep brain stimulation in human Parkinson’s disease patients,” said Philip Starr, M.D., Ph.D., professor of neurological surgery, University of California, San Francisco, and senior author of the study, which was published in the Journal of Neural Engineering.

Keyword: Parkinsons
Link ID: 25034 - Posted: 05.30.2018

A new neck brace for people with motor neurone disease (MND) makes a "substantial difference" to their quality of life, a patient has said. The disease causes muscle wasting, eventually leaving people with the condition unable to support their head. MND patient Philip Brindle said the collar, designed in Sheffield, "opened up opportunities that I do not think I would have had otherwise". The device is now being used by 25 NHS Trusts, according to its designers. MND is a progressive and terminal disease that damages the function of nerves and leads to muscle wasting and mobility problems, among other symptoms. It affects up to 5,000 adults in the UK, according to charity the MND Association. Dr Brian Dickie, director of research development at the association, said the collar has been "preferred by the majority of people who tried it". Image caption Mr Brindle's MND has left him unable to hold his head up independently Mr Brindle, 72, from Chesterfield, said since he was diagnosed with MND in 2015 his head had begun to drop and he did not want to be seen in public. "I just do not have the strength to hold [my head] up anymore and that makes life extremely unpleasant," he said. "You can't read, you can't watch TV, you can't have a conversation with anyone and you can't eat or drink with your head in that position." Image caption The Head Up collar is made from the same material used in space suits The new collar was designed by researchers at the University of Sheffield and Sheffield Hallam University, together with patients and clinicians at Sheffield Teaching Hospital. It has a soft fabric base, made from a material used by NASA to make space suits, on to which a series of shaped supports can be added to provide additional stability. © 2018 BBC

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25033 - Posted: 05.30.2018

By GINA KOLATA The first of a new class of drugs to prevent migraines was approved last week. The medication, called Aimovig, reduces the frequency of migraines among those severely afflicted, but the drug rarely prevents these episodes altogether. One expert called it “progress but not a panacea.” Migraine is the most disabling neurological disease in the world among people under age 50, beating epilepsy, strokes and chronic back pain. Yet many who have migraines don’t realize it or ever mention their symptoms to a doctor. Migraines are not just headaches. It is diagnosed in patients only if they have had a minimum of five attacks, each lasting four to 72 hours. Each attack has to include at least two of the following symptoms: throbbing headache with pain that is moderate to severe, that worsens with activity, and is only on only one side of the head. Also, a person suffering a migraine attack is nauseated or abhors sound or noise. What about auras? Are they part of a migraine? Sometimes, but not always. About 20 percent of migraine patients get an aura before the headache. Auras involve distortions of vision. People see jagged lights or have blind spots in their visual field. But auras can take other forms as well: a prickling pins-and-needles feeling on parts of the body, speech disturbances, distortions of sounds. Some get auras without a headache or only a mild headache. Auras actually involve different areas of the brain than migraines, and it is not clear why they are linked to migraine headaches. How common are migraines? They can start in childhood, although they usually begin in adolescence or young adulthood. They strike nearly one in five women worldwide, one in 16 men and one in 11 children. One out of four households has at least one member with migraine. The condition seems to spring from a combination of genetic and environmental factors. There is nothing a person can do to reduce the odds of developing migraine. © 2018 The New York Times Company

Keyword: Pain & Touch
Link ID: 25020 - Posted: 05.25.2018

By Emily Underwood *Update, 18 May, 10 a.m.: Yesterday, the U.S. Food and Drug Administration approved the first in a new class of drugs designed to prevent migraines. This feature, originally published on 7 January 2016, describes the history of these drugs, the powerful relief they can bring some patients, and the limitations that still exist with them. As long as she can remember, 53-year-old Rosa Sundquist has tallied the number of days per month when her head explodes with pain. The migraines started in childhood and have gotten worse as she’s grown older. Since 2008, they have incapacitated her at least 15 days per month, year-round. Head-splitting pain isn’t the worst of Sundquist’s symptoms. Nausea, vomiting, and an intense sensitivity to light, sound, and smell make it impossible for her to work—she used to be an office manager—or often even to leave her light-proofed home in Dumfries, Virginia. On the rare occasions when she does go out to dinner or a movie with her husband and two college-aged children, she wears sunglasses and noise-canceling headphones. A short trip to the grocery store can turn into a full-blown attack “on a dime,” she says. Every 10 weeks, Sundquist gets 32 bee sting–like injections of the nerve-numbing botulism toxin into her face and neck. She also visits a neurologist in Philadelphia, Pennsylvania, who gives her a continuous intravenous infusion of the anesthetic lidocaine over 7 days. The lidocaine makes Sundquist hallucinate, but it can reduce her attacks, she says—she recently counted 20 migraine days per month instead of 30. Sundquist can also sometimes ward off an attack with triptans, the only drugs specifically designed to interrupt migraines after they start. © 2018 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 24996 - Posted: 05.19.2018

By Gina Kolata The first medicine designed to prevent migraines was approved by the Food and Drug Administration on Thursday, ushering in what many experts believe will be a new era in treatment for people who suffer the most severe form of these headaches. The drug, Aimovig, made by Amgen and Novartis, is a monthly injection with a device similar to an insulin pen. The list price will be $6,900 a year, and Amgen said the drug will be available to patients within a week. Aimovig blocks a protein fragment, CGRP, that instigates and perpetuates migraines. Three other companies — Lilly, Teva and Alder — have similar medicines in the final stages of study or awaiting F.D.A. approval. “The drugs will have a huge impact,” said Dr. Amaal Starling, a neurologist and migraine specialist at the Mayo Clinic in Phoenix. “This is really an amazing time for my patient population and for general neurologists treating patients with migraine.” Millions of people experience severe migraines so often that they are disabled and in despair. These drugs do not prevent all migraine attacks, but can make them less severe and can reduce their frequency by 50 percent or more. As a recent editorial in the journal JAMA put it, they are “progress, but not a panacea.” Until now, drugs used to prevent migraines were designed to treat other diseases, like high blood pressure. They are not very effective, may work only temporarily, and often are laden with intolerable side effects. In clinical trials, people taking the new drugs reported no more side effects than those taking a placebo. The side effects over the long term and among people with chronic diseases remain to be determined. © 2018 The New York Times Company

Keyword: Pain & Touch
Link ID: 24994 - Posted: 05.18.2018

Prion diseases are slow degenerative brain diseases that occur in people and various other mammals. No vaccines or treatments are available, and these diseases are almost always fatal. Scientists have found little evidence of a protective immune response to prion infections. Further, microglia — brain cells usually involved in the first level of host defense against infections of the brain — have been thought to worsen these diseases by secreting toxic molecules that can damage nerve cells. Now, scientists have used an experimental drug, PLX5622, to test the role of microglia against scrapie, a prion disease of sheep. PLX5622 rapidly kills most of the microglia in the brain. When researchers gave the drug to mice infected with scrapie, microglia were eliminated and the mice died one month faster than did untreated mice. The results, published in the Journal of Virology by researchers from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, suggest that microglia can defend against a prion infection and thus slow the course of disease. The scientists hypothesize that microglia trap and destroy the aggregated prion proteins that cause brain damage. The findings suggest that drugs that increase the helpful activity of microglia may have a role in slowing the progression of prion diseases. Researchers are now studying the details of how microglia may be able to destroy prions in the brain. The scientists note that microglia could have a similar beneficial effect on other neurodegenerative diseases associated with protein aggregation, such as Alzheimer’s disease and Parkinson’s disease.

Keyword: Prions; Glia
Link ID: 24991 - Posted: 05.18.2018

By Shawna Williams Even as patients with Parkinson’s disease, obsessive-compulsive disorder, and other conditions turn to deep brain stimulation (DBS) to keep their symptoms in check, it’s been unclear to scientists why the therapy works. Now, researchers in Texas report that in mice, the treatment dials the activity of hundreds of genes up or down in brain cells. Their results, published in eLife March 23, hint that DBS’s use could be expanded to include improving learning and memory in people with intellectual disabilities. “The paper is very well done. . . . It’s really a rigorous study,” says Zhaolan “Joe” Zhou, a neuroscientist at the University of Pennsylvania’s Perelman School of Medicine who reviewed the paper for eLife. Now that the genes and pathways DBS affects are known, researchers can home in on ways to improve the treatment, or perhaps combine the therapy with pharmacological approaches to boost its effect, he says. In DBS, two electrodes are surgically implanted in a patient’s brain (the area depends on the disorder being treated), and connected to generators that are placed in the chest. Gentle pulses of electricity are then passed continuously through the electrodes. The treatment reduces motor symptoms in many people with Parkinson’s, and allows some patients to reduce their use of medications, but it does not eliminate symptoms or slow the disease’s progression. In addition to its use in movement disorders, DBS is being explored as a potential therapy for a range of other brain-related disorders. For instance, as a way to boost learning and memory in people with Alzheimer’s disease, researchers are looking into stimulating the fimbria-fornix, a brain region thought to regulate the activity of the memory-storing hippocampus. © 1986-2018 The Scientist

Keyword: Parkinsons; Epigenetics
Link ID: 24982 - Posted: 05.16.2018

A new tool developed by researchers at the National Institutes of Health has determined, for the first time, how two distinct sets of neurons in the mouse brain work together to control movement. The method, called spectrally resolved fiber photometry (SRFP), can be used to measure the activity of these neuron groups in both healthy mice and those with brain disease. The scientists plan to use the technique to better understand what goes wrong in neurological disorders, such as Parkinson’s disease. The study appeared online in the journal Neuron. According to Guohong Cui, M.D., Ph.D., head of the In Vivo Neurobiology Group at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, the project began because he wanted to find out why patients with Parkinson’s disease have problems with movement. Typically, the disease motor symptoms include tremor, muscle stiffness, slowness of movement, and impaired balance. Cui explained that an animal’s ability to move was controlled by two groups of neurons in the brain called the direct pathway (D1) and indirect pathway (D2). Based on clinical studies of patients with Parkinson’s and primate models, some researchers hypothesized that the loss of the neurotransmitter dopamine in the midbrain resulted in an imbalance of neural activities between D1 and D2. Since previous methods could not effectively distinguish different cell types in the brain, the hypothesis remained under debate. However, using SRFP, Cui’s team was able to label D1 and D2 neurons with green and red fluorescent sensors to report their neural activity.

Keyword: Parkinsons; Movement Disorders
Link ID: 24976 - Posted: 05.15.2018

By Ashley Yeager At first glance, neurons and muscle cells are the stars of gross motor function. Muscle movement results from coordination between nerve and muscle cells: when an action potential arrives at the presynaptic neuron terminal, calcium ions flow, causing proteins to fuse with the cell membrane and release some of the neuron’s contents, including acetylcholine, into the cleft between the neuron and muscle cell. Acetylcholine binds to receptors on the muscle cell, sending calcium ions into it and causing it to contract. But there’s also a third kind of cell at neuromuscular junctions, a terminal/perisynaptic Schwann cell (TPSC). These cells are known to aid in synapse formation and in the repair of injured peripheral motor axons, but their possible role in synaptic communications has been largely ignored. Problems with synaptic communication can underlie muscle fatigue, notes neuroscientist Thomas Gould of the University of Nevada, Reno, in an email to The Scientist. “Because these cells are activated by synaptic activity, we wondered what the role of this activation was.” To investigate, he and his colleagues stimulated motor neurons from neonatal mouse diaphragm tissue producing a calcium indicator, and found that TPSCs released calcium ions from the endoplasmic reticulum into the cytosol and could take in potassium ions from the synaptic cleft between neurons and muscle cells. However, TPSCs lacking the protein purinergic 2Y1 receptor (P2Y1R) didn’t release calcium or appear to take in potassium ions. © 1986-2018 The Scientist

Keyword: Glia; Muscles
Link ID: 24964 - Posted: 05.12.2018

Katie Nicholson, Joanne Levasseur Cannabidiol oil, or CBD, is generating a lot of buzz in the world of alternative medicine and many Canadians are buying in. The oil, which is extracted from marijuana plants, doesn't have the same mind-altering effects as smoking pot. People rub it on their achy joints or put it under their tongue to help them sleep. Some purveyors say it's completely legal in Canada and can be used for a long list of ailments, including epilepsy and multiple sclerosis. But federal authorities say CBD oil, which is widely available at head shops and online, is indeed illegal without a medical marijuana prescription. And its purported health benefits are also still in question. Cannabis products not yet legal Canadian affiliates of HempWorx, a multi-level marketing company based in Las Vegas, have been pushing CBD oil products through websites that say the product is allowed in Canada. They also list how much people should take for a long list of diseases. HempWorx did not respond to multiple interview requests. But in April, one of its Winnipeg-based affiliates told CBC News that its sale is "100 per cent legal." Under current Canadian law, the possession or sale of cannabidiol oil is illegal the same way other cannabis products are illegal. The same goes for importing or exporting the substance. The fact that it doesn't get you high doesn't matter. ©2018 CBC/Radio-Canada.

Keyword: Drug Abuse; Pain & Touch
Link ID: 24961 - Posted: 05.11.2018

A new discovery shows that opioids used to treat pain, such as morphine and oxycodone, produce their effects by binding to receptors inside neurons, contrary to conventional wisdom that they acted only on the same surface receptors as endogenous opioids, which are produced naturally in the brain. However, when researchers funded by the National Institute on Drug Abuse (NIDA) used a novel molecular probe to test that common assumption, they discovered that medically used opioids also bind to receptors that are not a target for the naturally occurring opioids. NIDA is part of the National Institutes of Health. This difference between how medically used and naturally made opioids interact with nerve cells may help guide the design of pain relievers that do not produce addiction or other adverse effects produced by morphine and other opioid medicines. “This ground-breaking study has uncovered important distinctions between the opioids that our brain makes naturally and therapeutic opioids that can be misused,” said NIDA Director Nora D. Volkow, M.D. “This information can be mined to better understand the potential adverse actions of medically prescribed opioids and how to manipulate the endogenous system to achieve optimal therapeutic results without the unhealthy side effects of tolerance, dependence, or addiction.” Naturally occurring opioids and medically used opioids alike bind to the mu-opioid receptor, a member of a widespread family of proteins known as G protein-coupled receptors (GPCRs). Recent advances in understanding the three-dimensional structure of GPCRs have enabled researchers to create a new type of antibody biosensor, called a nanobody, that generates a fluorescent signal when a GPCR is activated. This enables scientists to track chemicals as they move through cells and respond to stimuli.

Keyword: Pain & Touch; Drug Abuse
Link ID: 24960 - Posted: 05.11.2018