Chapter 5. The Sensorimotor System

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By GRETCHEN REYNOLDS Exercise may help the brain to build durable memories, through good times and bad. Stress and adversity weaken the brain’s ability to learn and retain information, earlier research has found. But according to a remarkable new neurological study in mice, regular exercise can counteract those effects by bolstering communication between brain cells. Memory has long been considered a biological enigma, a medley of mental ephemera that has some basis in material existence. Memories are coded into brain cells in the hippocampus, the brain’s memory center. If our memories were not written into those cells, they would not be available for later, long-term recall, and every brain would be like that of Dory, the memory-challenged fish in “Finding Nemo.” But representations of experience are extremely complex, and aspects of most memories must be spread across multiple brain cells, neuroscientists have determined. These cells must be able to connect with one another, so that the memory, as a whole, stays intact. The connections between neurons, known as synapses, are composed of electrical and chemical signals that move from cell to cell, like notes passed in class. The signals can be relatively weak and sporadic or flow with vigor and frequency. In general, the stronger the messages between neurons, the sturdier and more permanent the memories they hold. Neuroscientists have known for some time that the potency of our synapses depends to some degree on how we live our lives. Lack of sleep, alcohol, diet and other aspects of our lifestyles, especially stress, may dampen the flow of messages between brain cells, while practice fortifies it. Repeat an action and the signals between the cells maintaining the memory of that action can strengthen. That is learning. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24683 - Posted: 02.21.2018

by Sandra G. Boodman “What are you doing ?” Laura Hsiung’s friends asked as she slowly loped across a Maryland handball court, her ankle off-kilter so that she was walking on the outside of her left foot. Hsiung recalls wondering the same thing. One minute she was walking normally, and then all of a sudden, she wasn’t. “I couldn’t figure it out,” Hsiung said. “I hadn’t rolled my ankle. But my left foot just would not function normally.” For the next two years, Hsiung consulted specialist after specialist — orthopedists, a podiatrist and a neurologist — each of whom was unable to explain what was causing her weird walk. She underwent surgery which didn’t help and felt increasingly desperate about the problem, which did not affect her right foot. “Doctors would literally say, ‘I don’t know what’s wrong with you,’ ” said Hsiung, who lives in Montgomery County. Nor, she said, did most of them seem interested in unearthing a probable cause. After nearly two years of frustration and anxiety, a consultation with a physical therapist ultimately led to a diagnosis, followed by treatment that has helped alleviate Hsiung’s unusual disorder. Although they met only twice, the impact of her encounters with that physical therapist had a galvanizing effect on another aspect of Hsiung’s life, pushing her to make a midlife career change she had been contemplating. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 24677 - Posted: 02.19.2018

Dan Garisto If you’ve ever felt the urge to tap along to music, this research may strike a chord. Recognizing rhythms doesn’t involve just parts of the brain that process sound — it also relies on a brain region involved with movement, researchers report online January 18 in the Journal of Cognitive Neuroscience. When an area of the brain that plans movement was disabled temporarily, people struggled to detect changes in rhythms. The study is the first to connect humans’ ability to detect rhythms to the posterior parietal cortex, a brain region associated with planning body movements as well as higher-level functions such as paying attention and perceiving three dimensions. “When you’re listening to a rhythm, you’re making predictions about how long the time interval is between the beats and where those sounds will fall,” says coauthor Jessica Ross, a neuroscience graduate student at the University of California, Merced. These predictions are part of a system scientists call relative timing, which helps the brain process repetitive sounds, like a musical rhythm. “Music is basically sounds that have a structure in time,” says Sundeep Teki, a neuroscientist at the University of Oxford who was not involved with the study. Studies like this, which investigate where relative timing takes place in the brain, could be crucial to understanding how the brain deciphers music, he says. |© Society for Science & the Public 2000 - 2018.

Keyword: Hearing
Link ID: 24675 - Posted: 02.17.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Prions
Link ID: 24665 - Posted: 02.15.2018

National Institutes of Health scientists developing a rapid, practical test for the early diagnosis of prion diseases have modified the assay to offer the possibility of improving early diagnosis of Parkinson’s disease and dementia with Lewy bodies. The group, led by NIH’s National Institute of Allergy and Infectious Diseases (NIAID), tested 60 cerebral spinal fluid samples, including 12 from people with Parkinson’s disease, 17 from people with dementia with Lewy bodies, and 31 controls, including 16 of whom had Alzheimer’s disease. The test correctly excluded all the 31 controls and diagnosed both Parkinson’s disease and dementia with Lewy bodies with 93 percent accuracy. Importantly, test results were available within two days, compared to related assays that require up to 13 days. The group conducted the tests using Real-Time Quaking-Induced Conversion (RT-QuIC), an assay developed and refined over the past decade at NIAID’s Rocky Mountain Laboratories. Scientists from the University of California San Diego, University of Verona in Italy, Indiana University School of Medicine, Indianapolis, and the Case Western Reserve University School of Medicine, Cleveland, collaborated on the project. The research findings were published in Acta Neuropathologica Communications. Multiple neurological disorders, including Parkinson’s disease and dementia with Lewy bodies, involve the abnormal clumping of a protein called alpha-synuclein into brain deposits called Lewy bodies. The pathological processes in these diseases resembles prion diseases in mammal brains. Like prion diseases, Parkinson’s disease and dementia with Lewy bodies result in progressive deterioration of brain functions and, ultimately, death. Parkinson’s disease is about 1,000 times more common than prion diseases, affecting up to 1 million people in the United States, with 60,000 new cases diagnosed each year. Lewy body dementia affects an estimated 1.4 million people in the United States, according to the Lewy Body Dementia Association.

Keyword: Movement Disorders; Parkinsons
Link ID: 24641 - Posted: 02.10.2018

By Kimberly Hickok Your webcam may know your face, but your keyboard knows your gender. Computer models can predict with 95.6% accuracy whether a man or woman is typing, according to a new study. To conduct the research, computer engineers installed keystroke-logging software onto the personal computers of 75 volunteers—36 men, 39 women—which monitored their daily computer use for 10 months. The researchers then used a program they created, called “ISqueezeU” to calculate the relative helpfulness of different typing features for determining gender—things like the time between two specific keystrokes, or the amount of time a key is pressed down during a single keystroke. A few features stood out as being more useful than others. For example, the average time between pressing the “N” key to pressing the “O” key was the most helpful, followed by the average time between pressing the “M” and “O” keys. The program isn’t capable of specifying whether a man or woman types those keys faster or more often—only that there is a difference. The researchers then tested the program’s findings using five machine learning models, which are computer programs that build models based on what they “learn” from existing data. All five models were able to predict gender accurately more than 78% of the time, with the most successful model being more than 95% accurate, the engineers report this week in Digital Investigation. The team proposes the use of keystroke dynamics as a cost-efficient and nonintrusive way to identify the gender of unknown computer users in criminal investigations, such as in cases of cyberstalking or identity theft. The researchers plan to expand their data collection with more volunteers, and see whether incorporating other variables such as handedness or education level can increase accuracy. © 2018 American Association for the Advancement of Science

Keyword: Sexual Behavior
Link ID: 24639 - Posted: 02.10.2018

By LISA SANDERS, M.D. “Something’s wrong,” the woman told the young doctor, her face lined with worry. “This is not my husband.” The 68-year-old man lay unmoving in the hospital bed, his eyes dull, his face expressionless. His wife stood by him, as she had for nearly four decades of marriage. You don’t know him, she said, but if you did, you’d know that something is not right. George Goshua, a doctor in his first year of residency, looked at the distressed woman and then back at the man in the bed. He had spent nearly an hour reviewing the man’s hospital chart before coming to see him, and he knew the patient had been dangerously ill in the intensive-care unit for the last week. It all began about two weeks before, the wife explained. They were preparing for their son’s wedding, and her husband, normally a workhorse, was not feeling well. He was a tough guy — he worked as an estimator for a local builder and constructed his own house pretty much single-handedly. But now he said he was exhausted. At one point, just two days before the wedding, he said, “I think I might die.” At the time, she was irritated, because she thought he was just trying to get out of the work. Now she knew otherwise. They made it through the wedding, but the next day he was a wreck. His neck was stiff, as if there were a crick on both sides. He went to the local urgent-care center. They thought it was probably just a sore muscle and gave him something for the pain. The day after that, he had a fever. And the following day he was so weak he couldn’t walk. When his wife realized he was too sick to see his own doctor, she called an ambulance. As she struggled to get him out of his pajamas and into his clothes, he slid off the couch onto the floor. He just lay there, unable to even sit up. She couldn’t lift him. When the E.M.T.s arrived, they loaded him into an ambulance, and she followed them to Yale New Haven Hospital, in New Haven, Conn. © 2018 The New York Times Company

Keyword: Movement Disorders
Link ID: 24621 - Posted: 02.06.2018

Ian Sample Science editor A nasal spray that delivers a natural painkiller to the brain could transform the lives of patients by replacing the dangerous and addictive prescription opioids that have wreaked havoc in the US and claimed the lives of thousands of people. Scientists at University College London found they could alleviate pain in animals with a nasal spray that delivered millions of soluble nanoparticles filled with a natural opioid directly into the brain. In lab tests, the animals showed no signs of becoming tolerant to the compound’s pain-relieving effects, meaning the risk of overdose should be far lower. The researchers are now raising funds for the first clinical trial in humans to assess the spray’s safety. They will start with healthy volunteers who will receive the nasal spray to see if it helps them endure the pain of immersing one of their arms in ice-cold water. “If people don’t develop tolerance, you don’t have them always having to up the dose. And if they don’t have to up the dose, they won’t get closer and closer to overdose,” said Ijeoma Uchegbu, a professor of pharmaceutical nanoscience who is leading the research through Nanomerics, a UCL startup. If the first human safety trial is successful, the scientists will move on to more trials to investigate whether the nasal spray can bring swift relief to patients with bone cancer who experience sudden and excruciating bouts of pain.

Keyword: Pain & Touch; Drug Abuse
Link ID: 24609 - Posted: 02.03.2018

By NICHOLAS BAKALAR Having migraine headaches increases the risk for cardiovascular diseases, a new study has found. Using the Danish National Patient Registry, researchers matched 51,032 people with migraines, 71 percent of them women, with 510,320 people in the general population without migraines. The subjects were, on average, age 35 at the start of the study, and researchers followed them for 19 years. The absolute risk for cardiovascular disease was small, unsurprising in a group this young. Nevertheless, after adjustment for other variables, over the course of the study people with migraines had a 49 percent increased chance of heart attack, and roughly double the risk of stroke. They also had a 59 percent increased risk of a blood clot in their veins. These risks were even higher in the first year after a migraine diagnosis. The observational study, in BMJ, found no association of migraine with peripheral artery disease or heart failure. “We now have accumulating evidence that migraine is a risk factor for cardiovascular disease. It’s important to take it into consideration,” said the lead author, Dr. Kasper Adelborg, a postdoctoral researcher at Aarhus University. “And it’s important to find out if the agents that prevent migraine could also reduce the burden of cardiovascular disease.” © 2018 The New York Times Company

Keyword: Stroke; Pain & Touch
Link ID: 24597 - Posted: 02.01.2018

By Shawna Williams When the late organic chemist John Daly was on the hunt for poisonous frogs, he employed an unadvisable method: “It involved touching the frog, then sampling it on the tongue. If you got a burning sensation, then you knew this was a frog you ought to collect,” he once told a National Institutes of Health (NIH) newsletter writer. Daly survived to gather frogs from South America, Madagascar, Australia, and Thailand, and he extracted more than 500 compounds from their skin (many of which the frogs in turn had harvested from their insect diets). One of these compounds, the toxin epibatidine, turned out to have an analgesic effect 200 times more potent than morphine in rodents, Daly and his colleagues reported in 1992 (J Am Chem Soc, 114:3475-78, 1992); and rather than working through opioid receptors, epibatidine bound to nicotinic receptors. “To have a drug that works as well [as opioids] but is actually targeting a completely independent receptor system is really one of those holy grails of the drug industry,” says Daniel McGehee, who studies nicotinic receptors at the University of Chicago. But an epibatidine-related compound tested by Abbott Labs as an analgesic in the late 2000s caused uncontrollable vomiting, McGehee says. Although research on nicotinic receptors continues, he’s not aware of any epibatidine analogs currently in the drug development pipeline. But frogs may yet hold clues to killing pain. At least one frog does deploy an opioid: the waxy monkey tree frog (Phyllomedusa sauvagii), whose skin is laced with the peptide dermorphin. Although the compound does not appear to be a toxin that wards off predators, dermorphin has about 40 times the potency of morphine in a guinea-pig ileum assay, but it doesn’t effectively cross the blood-brain barrier, says pharmacologist Tony Yaksh of the University of California, San Diego. Dermorphin also boasts an unusual chemical property: the inclusion of a D-amino acid in its sequence. Almost all amino acids found in natural compounds are L-isomers, and dermorphin’s stereochemistry makes it resistant to metabolism and “certainly renders it more potent,” Yaksh writes in an email to The Scientist. © 1986-2018 The Scientist

Keyword: Pain & Touch; Drug Abuse
Link ID: 24577 - Posted: 01.27.2018

By Katarina Zimmer | Cellular senescence, the process by which cells cease to divide in response to stress, may be a double-edged sword. In addition to being an important anti-cancer mechanism, recent studies show it may also contribute to age-related tissue damage and inflammation. A study published in Cell Reports yesterday (January 23) suggests that cellular senescence could be a factor underlying neurodegeneration in sporadic forms of Parkinson’s disease. “I think the proposition that cellular senescence drives neurodegeneration in Parkinson’s disease and other ageing-related neurodegenerative diseases . . . has a great deal of merit,” writes D James Surmeier, a physiologist at Northwestern University, to The Scientist in an email. “To my knowledge, [this study] is the first strong piece of evidence for this model.” Cellular senescence may be the basis by which the herbicide and neurotoxin paraquat, which has been previously linked to Parkinson’s disease, can contribute to the disease, the researchers propose. The vast majority of Parkinson’s disease cases are sporadic, rather than inherited, and caused by a combination of environmental and genetic factors. Julie Andersen, a neuroscientist at the Buck Institute for Research on Aging, says her laboratory decided to focus on paraquat based on epidemiological evidence linking it to the condition in humans and on lab work showing that mice treated with the chemical suffer a loss of dopaminergic neurons in the same region that is affected in humans. It is an acutely toxic chemical—capable of causing death—and was banned in the E.U. in 2007 over safety concerns, but is still used extensively by American farmworkers. © 1986-2018 The Scientist

Keyword: Parkinsons; Glia
Link ID: 24574 - Posted: 01.26.2018

Ian Sample Science editor In work that could open a new front in the war on Parkinson’s disease, and even ageing itself, scientists have shown that they can stave off some of the effects of the neurodegenerative disease by flushing “zombie cells” from the brain. The research in mice raises hopes for a fresh approach to treating the most common forms of Parkinson’s disease, which typically arise through a complex interplay of genetics, lifestyle and potentially toxic substances in the environment. But the approach may have benefits far beyond Parkinson’s, with other neurodegenerative diseases – and the ageing process more broadly – all being linked to the ill effects of these “senescent” cells, which linger in tissues after entering a state of suspended animation in the body. “It’s a completely new way of looking at neurodegenerative disease and finding potential drugs,” said Marco Demaria, a molecular biologist on the team at the University of Groningen in the Netherlands. “For most of these conditions, we don’t have any way to counteract them.” Parkinson’s disease affects about 10 million people worldwide, and usually takes hold when certain types of neurons in the brain become impaired or die off completely. The neurons in question produce a substance called dopamine, which is crucial for enabling the brain to produce smooth and coordinated physical movements. © 2018 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 24562 - Posted: 01.24.2018

By Abby Olena Studying scorpions comes with its share of danger, as biologist Bryan Fry of the University of Queensland knows all too well. On a 2009 trip to the Brazilian Amazon, Fry was stung while trying to collect the lethal Brazilian yellow scorpion (Tityus serrulatus), and for eight hours he says it felt as though his finger was in a candle flame. Meanwhile, his heart flipped between racing and stopping for up to five seconds at a time. “At least the insane levels of pain helped keep my mind off my failing heart,” Fry writes in an email to The Scientist. His symptoms were caused by an arsenal of toxins in the animal’s sting, which contribute to one of the most painful attacks in the animal kingdom. But at least one mammal—the southern grasshopper mouse (Onychomys torridus)—regularly chows down on Arizona bark scorpions (Centruroides sculpturatus) and doesn’t seem to experience pain, despite receiving plenty of stings. In 2013, Ashlee Rowe, now of Michigan State University, and colleagues showed that bark scorpion venom interacts with the NaV1.8 voltage-gated sodium channel in grasshopper mice, in addition to activating the NaV1.7 channel as it does in other mammals (Science, 342:441-46). Rowe’s team showed that grasshopper mice have evolved amino acid changes in NaV1.8 that allow it to bind scorpion venom components, and in turn prevent the channel’s activation. Because NaV1.8 is responsible for transmitting pain signals to the central nervous system following NaV1.7 binding, blocking its activation prevents the sensation of pain. In other mammals, scorpion venom has no effect on NaV1.8. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24557 - Posted: 01.24.2018

By Jenny Rood Opioid drugs are well-established double-edged swords. Extremely effective at analgesia, they cause an array of harmful side effects throughout the body, including itching, constipation, and respiratory depression—the slowed breathing that ultimately causes death in overdose cases. What’s more, the body’s interaction with opioids is dynamic: our receptors for these compounds become desensitized to the drugs’ activity over time, requiring ever larger doses to suppress pain and eventually provoking severe dependence and protracted withdrawal. In the past few years, these side effects have plagued growing numbers of US citizens, plunging the country into the throes of a devastating opioid crisis in which nearly 100 people die from overdoses every day. Even so, opioids are still among the most effective pain-relief options available. “Over hundreds of years, [opioid receptors] have remained a target,” says Laura Bohn, a biochemist at the Scripps Research Institute in Jupiter, Florida. “Therapeutically, it works.” Since the early 2000s, intriguing evidence has emerged suggesting that opioids’ useful properties could be separated from their harmful attributes. (See “Pain and Progress,” The Scientist, February 2014.) In 2005, Bohn, then at the Ohio State University College of Medicine, and colleagues showed that shutting down one of the signaling pathways downstream of the opioid receptor targeted by morphine not only amped up the drug’s painkilling effects in mice, but also reduced constipation and respiratory depression (J Pharmacol Exp Ther, 314:1195-201). © 1986-2018 The Scientist

Keyword: Pain & Touch; Drug Abuse
Link ID: 24550 - Posted: 01.22.2018

By Kate Baggaley The pain came without warning. It was February of last year, and the man was eating dinner. He’d just reached for a glass of wine. “It really burned my mouth when I started to drink,” says Greg (the healthcare worker in Toronto asked for his name to be changed). The odd and disquieting sensation had no apparent cause—no burns or cuts or other injuries. Yet the burning and tingling Greg felt on his tongue and the roof of his mouth persisted. “It was very intense during the middle of the day and then subsided at nighttime,” he says. Perhaps, he was told when finally visiting the family doctor months later, the pain was related to a yeast infection on the tongue. But the prescribed anti-fungal medication made no difference. Next Greg saw a dentist, who found no abnormalities in his mouth and recommended he get a blood test to rule out an autoimmune disorder. Eventually, though, one of Greg’s doctors referred him to Miriam Grushka, an oral medicine specialist in Toronto. Grushka has spent decades studying and treating Greg's condition, which is called burning mouth syndrome. “People say they feel like they burnt their tongue on a cup of coffee, but the burning never went away,” says Grushka. “In the vast majority of cases it’s benign, but it’s very uncomfortable.” Each week, she sees around 15 patients who have burning mouth syndrome or similar conditions. These hallucinations, or phantoms, are characterized by a taste or feeling in the mouth that will not go away. Oral phantoms are often treatable, and are rooted not in the mouth but the brain. But much else about these phantom feelings is still a mystery. Grushka and other researchers are still unraveling why they happen and how to banish them. © 2018 Popular Science.

Keyword: Pain & Touch; Chemical Senses (Smell & Taste)
Link ID: 24548 - Posted: 01.22.2018

By Anna Azvolinsky David Julius entered the biochemistry graduate program at the University of California, Berkeley, in 1977. “It was all one foot in front of the other. I wasn’t trying to figure out what I would be doing in 10 years,” says the University of California, San Francisco (UCSF) professor of physiology. “When I arrived, I thought, ‘Classes are pretty much over. This is like a real job, and I can just go in the lab and do my thing.’” Julius joined the UC Berkeley lab of Jeremy Thorner, who was studying hormonal signaling and trying to understand how budding yeast cells switch mating type. Randy Schekman, a Berkeley researcher who worked on protein secretion and vesicular transport, served as Julius’s coadvisor. “What was great about Jeremy and Randy was that they were both trained as biochemists and then had decided to take advantage of the yeast genetic system to understand the biochemistry of cellular signaling.” Haploid yeast cells can be either “type a” or “type α,” and mate with cells of the opposite type. Julius worked on the synthesis of alpha factor, one of two mating hormones produced and secreted by yeast. His graduate studies produced three Cell papers. The first, published in 1983, reported that a class of enzymes, the dipeptidyl aminopeptidases, is necessary to cleave a longer precursor of alpha factor into the final 13-amino-acid peptide. To identify the specific dipeptidyl aminopeptidase and elucidate its role, Julius took advantage of yeast mutants, including one called ste13 (for sterile 13), which cannot produce normal alpha factor. It was the first time anyone had characterized the biochemical functioning of one of the yeast sterile mutants. © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24543 - Posted: 01.20.2018

By Esther Landhuis As the sun went down on a recent Friday, the hospital clinic buzzed with activity. “Loads of patients turned up without appointments,” says Sarah Tabrizi, a neurologist at University College London. It wasn’t just the typical post-holiday rush. Many rushed in, Tabrizi suspects, after hearing news last month about a potential new therapy for Huntington’s disease, a brain disorder that cripples the body and blurs speech and thinking, sometimes not too long after a person’s 30th birthday. Like other neurodegenerative disorders such as Lou Gehrig’s, Parkinson’s and Alzheimer’s, Huntington’s has no cure. Over decades biotech companies have poured billions of dollars into developing and testing pharmaceuticals for these devastating conditions, only to unleash storms of disappointment. Yet in December a ray of something approximating hope poked through when a California company released preliminary findings from its small Huntington’s study. Results from this early-stage clinical trial have not yet been published or reported at medical meetings. But some researchers have growing confidence that the drug should work for Huntington’s and perhaps other diseases with clear genetic roots. The initial data showed enough promise to convince Roche to license the drug from California-based Ionis Pharmaceuticals, which sponsored the recent Huntington’s trial. The pharma giant paid Ionis $45 million for the right to conduct further studies and work with regulatory agencies to bring the experimental therapy to market. © 2018 Scientific American

Keyword: Huntingtons
Link ID: 24536 - Posted: 01.17.2018

Richard Harris The results of an IQ test can depend on the gender of the person who's conducting the test. Likewise, studies of pain medication can be completely thrown off by the gender of the experimenter. This underappreciated problem is one reason that some scientific findings don't stand the test of time. Colin Chapman found out about this problem the hard way. He had traveled to Sweden on a Fulbright scholarship to launch his career in neuroscience. And he decided to study whether a nasal spray containing a hormone called oxytocin would help control obesity. The hormone influences appetite and impulsive behavior in obese men. "I was really excited about this project, from what I understood about how the brain works, I thought it was kind of a slam dunk," he says. Chapman set up the experiment and then left for a few years to attend Harvard Law School. When he returned, the findings were not at all what he expected, "and I was really disappointed because this was my baby, it was my big project going into neuroscience." But Chapman, who is now a graduate student at the University of Uppsala, says his idea turned out to be right after all. "There was another research group that around the same time came up with the same idea," he says. "And they ran basically the same project and they got exactly the results I was expecting to get." © 2018 npr

Keyword: Sexual Behavior; Pain & Touch
Link ID: 24517 - Posted: 01.11.2018

By Dina Fine Maron One evening this past fall a patient stumbled into the emergency room at Brigham and Women’s Hospital in Boston. “I don’t feel so…” she muttered, before losing consciousness. Her breathing was shallow and her pupils were pinpoints, typical symptoms of an opioid overdose. Her care team sprang into action. They injected her with 0.4 milligram of naloxone, an overdose antidote—but she remained unresponsive. They next tried one milligram, then two, then four. In total they used 12 milligrams in just five minutes, says Edward Boyer, the physician overseeing her care that night. Yet the patient still had trouble breathing. They put a tube down her throat and hooked her to a ventilator. Twenty minutes later she woke up—angry and in drug withdrawal, but alive. The patient, whose identifying details may have been altered to protect patient confidentiality, had apparently injected herself with a synthetic opioid such as fentanyl right outside of the hospital building. That gave her just enough time to seek help. But many users of synthetic opioids are not so lucky. These drugs, which bear little chemical resemblance to any opioid derived from the opium poppy, are much more powerful than poppy-based heroin and semisynthetic opioids such as oxycodone or hydrocodone. Thus, the standard dose of naloxone employed by first responders (and sold in bystander overdose kits) is often not potent enough to save a synthetic opioid user’s life. © 2018 Scientific American

Keyword: Drug Abuse; Pain & Touch
Link ID: 24505 - Posted: 01.09.2018

By Catherine Offord Neurobiologist John Wood has long been interested in how animals feel pain. His research at University College London (UCL) typically involved knocking out various ion channels important in sensory neuronal function from mouse models and observing the effects. But in the mid-2000s, a peculiar story about a boy in Pakistan opened up a new, and particularly human-centric, research path. The story was relayed by Geoff Woods, a University of Cambridge geneticist. “Geoff had been wandering round Pakistan looking for consanguineous families that had genes contributing to microcephaly,” Wood recalls. During his time there, “somebody came to see him and said that there was a child in the marketplace who was damaging himself for the tourists—and was apparently pain-free.” The boy would regularly stick knives through his arms and walk across burning coals, the stories went. Wood’s group at UCL had just published a paper describing a similarly pain-insensitive phenotype in mice genetically engineered to lack the voltage-gated sodium channel NaV1.7 in pain-sensing neurons, or nociceptors. NaV1.7 controls the passage of sodium ions into the cell—a key step in membrane depolarization and, therefore, a neuron’s capacity to propagate an action potential. Wood’s postdoc, Mohammed Nassar, had shown that mice lacking functional NaV1.7 in their nociceptors exhibited higher-than-normal pain thresholds; they were slower to withdraw a paw from painful stimuli and spent less time licking or biting it after being hurt.1 Having read the study, Cambridge’s Woods reached out to the group in London to discuss whether this same channel could help explain the bizarre behavior of the boy he’d heard about in Pakistan. © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24503 - Posted: 01.09.2018