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

Tina Hesman Saey In movies, exploring the body up close often involves shrinking to microscopic sizes and taking harrowing rides through the blood. Thanks to a new virtual model, you can journey through a three-dimensional brain. No shrink ray required. The Society for Neuroscience and other organizations have long sponsored the website BrainFacts.org, which has basic information about how the human brain functions. Recently, the site launched an interactive 3-D brain. A translucent, light pink brain initially rotates in the middle of the screen. With a click of a mouse or a tap of a finger on a mobile device, you can highlight and isolate different parts of the organ. A brief text box then pops up to provide a structure’s name and details about the structure’s function. For instance, the globus pallidus — dual almond-shaped structures deep in the brain — puts a brake on muscle contractions to keep movements smooth. Some blurbs tell how a structure got its name or how researchers figured out what it does. Scientists, for example, have learned a lot about brain function by studying people who have localized brain damage. But the precuneus, a region in the cerebral cortex along the brain’s midline, isn’t usually damaged by strokes or head injuries, so scientists weren’t sure what the region did. Modern brain-imaging techniques that track blood flow and cell activity indicate the precuneus is involved in imagination, self-consciousness and reflecting on memories. |© Society for Science & the Public 2000 - 2018

Keyword: Brain imaging
Link ID: 24502 - Posted: 01.09.2018

by Emilie Reas Functional MRI (fMRI) is one of the most celebrated tools in neuroscience. Because of their unique ability to peer directly into the living brain while an organism thinks, feels and behaves, fMRI studies are often devoted disproportionate media attention, replete with flashy headlines and often grandiose claims. However, the technique has come under a fair amount of criticism from researchers questioning the validity of the statistical methods used to analyze fMRI data, and hence the reliability of fMRI findings. Can we trust those flashy headlines claiming that “scientists have discovered the area of the brain,” or are the masses of fMRI studies plagued by statistical shortcomings? To explore why these studies can be vulnerable to experimental failure, in their new PLOS One study coauthors Henk Cremers, Tor Wager and Tal Yarkoni investigated common statistical issues encountered in typical fMRI studies, and proposed how to avert them moving forward. The reliability of any experiment depends on adequate power to detect real effects and reject spurious ones, which can be influenced by various factors including the sample size (or number of “subjects” in fMRI), how strong the real effect is (“effect size”), whether comparisons are within or between subjects, and the statistical threshold used. To characterize common statistical culprits of fMRI studies, Cremers and colleagues first simulated typical fMRI scenarios before validating these simulations on a real dataset. One scenario simulated weak but diffusely distributed brain activity, and the other scenario simulated strong but localized brain activity (Figure 1). The simulation revealed that effect sizes are generally inflated for weak diffuse, compared to strong localized, activations, especially when the sample size is small. In contrast, effect sizes can actually be underestimated for strong localized scenarios when the sample size is large. Thus, more isn’t always better when it comes to fMRI; the optimal sample size likely depends on the specific brain-behavior relationship under investigation.

Keyword: Brain imaging
Link ID: 24501 - Posted: 01.09.2018

Eric Nyquist for Quanta Magazine Brains, beyond their signature achievements in thinking and problem solving, are paragons of energy efficiency. The human brain’s power consumption resembles that of a 20-watt incandescent lightbulb. In contrast, one of the world’s largest and fastest supercomputers, the K computer in Kobe, Japan, consumes as much as 9.89 megawatts of energy — an amount roughly equivalent to the power usage of 10,000 households. Yet in 2013, even with that much power, it took the machine 40 minutes to simulate just a single second’s worth of 1 percent of human brain activity. Now engineering researchers at the California NanoSystems Institute at the University of California, Los Angeles, are hoping to match some of the brain’s computational and energy efficiency with systems that mirror the brain’s structure. They are building a device, perhaps the first one, that is “inspired by the brain to generate the properties that enable the brain to do what it does,” according to Adam Stieg, a research scientist and associate director of the institute, who leads the project with Jim Gimzewski, a professor of chemistry at UCLA. The device is a far cry from conventional computers, which are based on minute wires imprinted on silicon chips in highly ordered patterns. The current pilot version is a 2-millimeter-by-2-millimeter mesh of silver nanowires connected by artificial synapses. Unlike silicon circuitry, with its geometric precision, this device is messy, like “a highly interconnected plate of noodles,” Stieg said. And instead of being designed, the fine structure of the UCLA device essentially organized itself out of random chemical and electrical processes. All Rights Reserved © 2018

Keyword: Learning & Memory; Robotics
Link ID: 24500 - Posted: 01.08.2018

By HENRY ALFORD Here in the valley of my mid-50s, I try not to get into a swivet over my occasionally faulty memory: Sometimes the mind has a mind of its own. But when I read this chilling passage — “I am dementing. I am dementing. I am dementing.” — from Gerda Saunders’s recent memoir “Memory’s Last Breath: Field Notes on My Dementia,” I found myself starting to panic. In a world increasingly dominated by the Google/Apple/Facebook/Amazon hegemony, we hear a lot about the threat to privacy. But isn’t memory just as vulnerable? Now that, as the former New Republic editor Franklin Foer writes in “World Without Mind: The Existential Threat of Big Tech,” “our phone is an extension of our memory; we’ve outsourced basic functions to algorithms,” doesn’t the world seem like an ever-larger parking lot that has mysteriously swallowed our Toyota? Don’t we all wish, now more than ever, that acquaintances came equipped with their own “Previously on this series …” trailer? Mr. Foer and Ms. Saunders aren’t the only writers on this beat. Recent books by Robert Sapolsky, Michael Lemonick, Felicia Yap, Emily Barr, Dale Bredesen, Val Emmich, Oliver Sacks and Elizabeth Rosner, among others, have addressed the theme of non-historical memory. Last July alone, more than a dozen books specifically about the topic, most of them self-published, were released. You’d expect the themes of amnesia or powers of recall to be prevalent in thrillers or in memoirs by trauma survivors or over-beveraged rock stars, but even literary fiction is getting in on the act. In Rachel Khong’s sly, diaristic “Goodbye, Vitamin,” a 30-year-old who moves back home learns she has to care for a dementing father who has started leaving his pants in trees. In Alissa Nutting’s outrageous sex comedy “Made for Love,” a woman on the lam from her tech pioneer husband discovers that he has implanted a chip in her brain that allows him to download all her experiences. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24499 - Posted: 01.08.2018

By Nicole Edison Worried you might say something you regret when talking in your sleep? Your concerns may be justified: According to a recent study from France, your midnight mumblings may be more negative and insulting than what you say while awake. In the study, researchers found that sleep talkers said the word “no” four times as often in their sleep as when awake. And the f-word popped up during sleep talking more than 800 times more frequently than while awake. To study sleep talking, the researchers recorded nearly 900 nighttime utterances from about 230 adults during one or two consecutive nights in a sleep lab. Because sleep talking is a relatively rare event, the majority of people in the study had certain types of sleep disorders, or parasomnias, which are unusual behaviors that happen during sleep, the researchers noted. Once recorded, the nocturnal episodes were analyzed for such factors as wordiness, silences, tone, politeness and abusive language. These results were compared to see how sleep speech matched up to everyday spoken French in form and content. The researchers found that the majority (59 percent) of the nighttime utterances were unintelligible or nonverbal, including mumbling, whispering and laughing. But among the utterances that were intelligible, a surprising amount of what was said was offensive or aggressive: 24 percent contained negative content, 22 percent had “nasty” language and almost 10 percent contained the word “no” in some form. (By comparison, the word “no” accounted for 2.5 percent of awake language.) © 1996-2018 The Washington Post

Keyword: Sleep
Link ID: 24498 - Posted: 01.08.2018

Nicola Davis The prospect of a non-addictive alternatives to morphine and other opioids has moved a step closer as scientists say they have cracked a key challenge in developing safe and effective substitute painkillers. Overuse of highly addictive opioids has led to a health crisis across the world, especially in the US where more than 60,000 people died after overdoses in 2016 alone; president Donald Trump has declared the epidemic a public health emergency. Researchers looking for alternatives examined a receptor protein that interacts with opioids in the brain, and have now revealed its structure as it binds to a molecule related to morphine. While the structure of the receptor had previously been reported, this is the first time scientists have unveiled its structure as it interacts with a drug. The development, they say, could prove pivotal. The protein, known as the kappa opioid receptor, is one of four that interacts with opioids, but – crucially – while it can trigger pain-killing effects, it is not linked to problems including constipation, addiction risk and death as a result of overdose. “Tens of thousands of people are dying every year in the US because of opioid overdoses; in the last year more than 50,000 people died. That is as many as died in the Vietnam war in the US. It is a terrible, terrible crisis,” said Bryan Roth, co-author of the research from the University of North Carolina at Chapel Hill. © 2018 Guardian News and Media Limited

Keyword: Drug Abuse; Pain & Touch
Link ID: 24497 - Posted: 01.06.2018

By Meredith Wadman For the first time, scientists have produced evidence in living humans that the protein tau, which mars the brain in Alzheimer’s disease, spreads from neuron to neuron. Although such movement wasn’t directly observed, the finding may illuminate how neurodegeneration occurs in the devastating illness, and it could provide new ideas for stemming the brain damage that robs so many of memory and cognition. Tau is one of two proteins—along with β-amyloid—that form unusual clumps in the brains of people with Alzheimer’s disease. Scientists have long debated which is most important to the condition and, thus, the best target for intervention. Tau deposits are found inside neurons, where they are thought to inhibit or kill them, whereas β-amyloid forms plaques outside brain cells. Researchers at the University of Cambridge in the United Kingdom combined two brain imaging techniques, functional magnetic resonance imaging and positron emission tomography (PET) scanning, in 17 Alzheimer’s patients to map both the buildup of tau and their brains’ functional connectivity—that is, how spatially separated brain regions communicate with each other. Strikingly, they found the largest concentrations of the damaging tau protein in brain regions heavily wired to others, suggesting that tau may spread in a way analogous to influenza during an epidemic, when people with the most social contacts will be at greatest risk of catching the disease. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 24496 - Posted: 01.06.2018

Veronique Greenwood TSUKUBA, Japan—Outside the International Institute for Integrative Sleep Medicine, the heavy fragrance of sweet Osmanthus trees fills the air, and big golden spiders string their webs among the bushes. Two men in hard hats next to the main doors mutter quietly as they measure a space and apply adhesive to the slate-colored wall. The building is so new that they are still putting up the signs. The institute is five years old, its building still younger, but already it has attracted some 120 researchers from fields as diverse as pulmonology and chemistry and countries ranging from Switzerland to China. An hour north of Tokyo at the University of Tsukuba, with funding from the Japanese government and other sources, the institute’s director, Masashi Yanagisawa, has created a place to study the basic biology of sleep, rather than, as is more common, the causes and treatment of sleep problems in people. Full of rooms of gleaming equipment, quiet chambers where mice slumber, and a series of airy work spaces united by a spiraling staircase, it’s a place where tremendous resources are focused on the question of why, exactly, living things sleep. Ask researchers this question, and listen as, like clockwork, a sense of awe and frustration creeps into their voices. In a way, it’s startling how universal sleep is: In the midst of the hurried scramble for survival, across eons of bloodshed and death and flight, uncountable millions of living things have laid themselves down for a nice, long bout of unconsciousness. This hardly seems conducive to living to fight another day. “It’s crazy, but there you are,” says Tarja Porkka-Heiskanen of the University of Helsinki, a leading sleep biologist. That such a risky habit is so common, and so persistent, suggests that whatever is happening is of the utmost importance. Whatever sleep gives to the sleeper is worth tempting death over and over again, for a lifetime. (c) 2018 by The Atlantic Monthly Group.

Keyword: Sleep
Link ID: 24495 - Posted: 01.06.2018

Nancy Shute It's just a cold. But even though I know I'm not horribly ill, I feel this overwhelming need to skip work, ignore my family and retreat to the far corner of the sofa. I'm not being a wimp, it turns out. Those feelings are a real thing called sickness behavior, which is sparked by the body's response to infection. The same chemicals that tell the immune system to rush in and fend off invading viruses also tell us to slow down, skip the eating, drinking and sex, shun social interactions and rest. "Those messages are so powerful they can't be ignored," says Philip Chen, a rhinologist at the University of Texas, San Antonio. But that doesn't mean we don't try. Symptoms like a stuffy nose are obvious, Chen notes, but we're less aware that changes in mood and behavior are also part of our bodies' natural response to infection. It might behoove us to pay attention. There's plenty of evidence that having a cold impairs mood, alertness and working memory, and that brain performance falls off with even minor symptoms. But for most people, having a cold does not equal "take the week off." And that means many people work sick, even when it can put others in danger. A 2015 survey of food workers found that half "always" or "frequently' went to work while sick. © 2018 npr

Keyword: Neuroimmunology; Stress
Link ID: 24494 - Posted: 01.06.2018

By Joshua Rothman One day in the nineteen-eighties, a woman went to the hospital for cancer surgery. The procedure was a success, and all of the cancer was removed. In the weeks afterward, though, she felt that something was wrong. She went back to her surgeon, who reassured her that the cancer was gone; she consulted a psychiatrist, who gave her pills for depression. Nothing helped—she grew certain that she was going to die. She met her surgeon a second time. When he told her, once again, that everything was fine, she suddenly blurted out, “The black stuff—you didn’t get the black stuff!” The surgeon’s eyes widened. He remembered that, during the operation, he had idly complained to a colleague about the black mold in his bathroom, which he could not remove no matter what he did. The cancer had been in the woman’s abdomen, and during the operation she had been under general anesthesia; even so, it seemed that the surgeon’s words had lodged in her mind. As soon as she discovered what had happened, her anxiety dissipated. Henry Bennett, an American psychologist, tells this story to Kate Cole-Adams, an Australian journalist, in her book “Anesthesia: The Gift of Oblivion and the Mystery of Consciousness.” Cole-Adams hears many similar stories from other anesthesiologists and psychologists: apparently, people can hear things while under anesthesia, and can be affected by what they hear even if they can’t remember it. One woman suffers from terrible insomnia after her hysterectomy; later, while hypnotized, she recalls her anesthesiologist joking that she would “sleep the sleep of death.” Another patient becomes suicidal after a minor procedure; later, she remembers that, while she was on the table, her surgeon exclaimed, “She is fat, isn’t she?” In the nineteen-nineties, German scientists put headphones on thirty people undergoing heart surgery, then, during the operation, played them an abridged version of “Robinson Crusoe.” None of the patients recalled this happening, but afterward, when asked what came to mind when they heard the word “Friday,” many mentioned the story. In 1985, Bennett himself asked patients receiving gallbladder or spinal surgeries to wear headphones. A control group heard the sounds of the operating theatre; the others heard Bennett saying, “When I come to talk with you, you will pull on your ear.” When they met with him, those who’d heard the message touched their ears three times more often than those who hadn’t. © 2018 Condé Nast.

Keyword: Consciousness; Sleep
Link ID: 24493 - Posted: 01.05.2018

By Richard Stone Even 3 decades later, Seyed Naser Emadi's first encounter with nerve agents haunts him. In 1987, as a soldier fighting for Iran in its war with Iraq, he came across a hillside strewn with comrades killed by an Iraqi nerve agent, perhaps tabun or sarin. Unable to breathe, the victims had clawed at their necks to try to open a hole in their throats, recalls Emadi, now a dermatologist in Tehran. In fact, their windpipes were clear; the nerve agent had shut down control of breathing in the central nervous system. They "had no choice except death," he says. The long-term effects of nerve agents remain uncertain, but with the right antidotes, these poisons need not be an immediate death sentence. A few years after Emadi's experience, U.S. soldiers in 1991's Gulf War carried autoinjectors filled with drugs that—in principle—would keep them breathing and protect them from seizures if Iraqi forces again unleashed nerve agents. They never did, most historians agree, but the threat remains real today, as chemical attacks in Syria's ongoing civil war make clear. It is spurring urgent efforts to find better countermeasures, with several promising compounds in the pipeline. First synthesized by German chemists on the eve of World War II, nerve agents kill by binding to acetylcholinesterase (AChE), an enzyme that dismantles the neurotransmitter acetylcholine when it is released into synapses. One of the most efficient enzymes known, a single AChE molecule can hydrolyze 600,000 acetylcholine molecules per minute, says Palmer Taylor, a pharmacologist at the University of California, San Diego. © 2018 American Association for the Advancement of Science

Keyword: Neurotoxins
Link ID: 24492 - Posted: 01.05.2018

By Alfonso Serrano Elvis Alonzo began smoking cannabis as a last resort. Three years as a Marine Corps officer and 13 years with the Glendale Police Department in Arizona—where he was exposed to murders, suicides and people dying in his arms—had left him emotionally crippled. Toward the end of his police service, doctors diagnosed Alonzo with post-traumatic stress disorder and prescribed various medications to temper his nightmares and flashbacks. The drugs “turned me into a zombie,” he says. “I was so out of it that I couldn’t even drive, so they (the police department) had to medically retire me.” Alonzo stopped showering. His wife left him, and he nearly lost his house. Then a friend suggested he try marijuana to relieve his symptoms. “It’s been a godsend,” he says. “It curbs my anxiety, and it makes me sleep fantastic for at least four hours. It needs to be studied.” Thousands of military veterans have echoed Alonzo’s claim for years. They have pressured federal and state legislators to legalize medicinal cannabis and ease rules on research into the plant’s apparent therapeutic properties, arguing that it could help reduce suicide rates among former soldiers. Backed by overwhelming public support for broader legalization, their demands are starting to resonate in statehouses across the country. This past November, New York Gov. Andrew Cuomo chose Veterans Day to make PTSD a qualifying condition for the state’s tightly controlled medical marijuana program. New York joined seven other states this year—and 27 overall—that include PTSD in their lists of conditions that qualify for medical cannabis. © 2018 Scientific America

Keyword: Drug Abuse; Stress
Link ID: 24491 - Posted: 01.05.2018

/ By Robin Lloyd Most Americans drink safely and in moderation, as many of us could attest earlier this week. But a steady annual increase in trips made to emergency rooms as a result of drinking alcohol added up to 61 percent more visits in 2014 compared with 2006, according to a study published this week in the journal Alcoholism: Clinical and Experimental Research. The increase is alarming but also a bit mysterious to neuroscientist Aaron White, one of the study’s authors, in part because the same nine-year period showed a mere 2 percent increase in per capita alcohol consumption overall, and an 8 percent increase in the number of emergency room visits for any reason. White and his four co-authors, three of whom work with him at the National Institute on Alcohol Abuse and Alcoholism, have yet to understand what’s behind the dramatic increase in alcohol-related ER visits. “The lowest hanging fruit in terms of hypotheses is that there must be an increase in risky drinking in some people,” White says. “Even though that is not showing up in increases in overall per capita consumption, it’s enough to drive the increase in alcohol-related emergency department visits.” But there is no strong evidence for a national increase in binge drinking, he added. The new finding comes from an analysis of a nationally representative data set that includes information on about 30 million visits to U.S. hospital-based emergency departments annually, from 945 hospitals in 33 states and Washington, D.C. Copyright 2018 Undark

Keyword: Drug Abuse
Link ID: 24490 - Posted: 01.05.2018

By RONI CARYN RABIN A. Studies have found a link between low levels of magnesium, an essential mineral that plays a crucial role in a wide range of bodily processes, and sleep disorders. But if you are concerned you aren’t getting enough magnesium, changing your diet may be a better option than taking a supplement, as “there is really sparse evidence that taking super-therapeutic doses of magnesium will give you a benefit,” said Dr. Raj Dasgupta, a professor of pulmonary and sleep medicine at the University of Southern California. The mineral is widely available in both plant and animal-based foods, and the kidneys limit urinary excretion of magnesium, so deficiencies are rare in healthy people. Leafy green vegetables, nuts, legumes and whole grains are good sources of magnesium; fish, chicken and beef also contain magnesium. Older adults and people with certain disorders, such as Type 2 diabetes, gastrointestinal diseases and alcoholism, however, may have inadequate amounts. “Magnesium deficiency has been associated with higher levels of stress, anxiety and difficulty relaxing, which are key ingredients to getting good sleep at night,” Dr. Dasgupta said. He noted that magnesium interacts with an important neurotransmitter that favors sleep. One small double-blinded clinical trial of 43 elderly people in Tehran who were randomly assigned to receive either 500 milligrams of magnesium or a placebo for eight weeks found that those who received the supplement fell asleep faster and spent more of their time in bed asleep, but their total sleep time was not necessarily longer. An even smaller study of 10 people done nearly 20 years ago found that taking a magnesium supplement helped people with restless leg syndrome get more sleep. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 24489 - Posted: 01.05.2018

By Meredith Wadman Chya* (pronounced SHY-a), who is not quite 10 years old, recently spent an unusual day at the University of Maryland School of Medicine in Baltimore. Part of the time she was in a "cool" brain scanner while playing video games designed to test her memory and other brain-related skills. At other points, she answered lots of questions about her life and health on an iPad. A slender Baltimore third grader who likes drawing, hip hop, and playing with her pet Chihuahua, Chya is one of more than 6800 children now enrolled in an unprecedented examination of teenage brain development. The Adolescent Brain Cognitive Development Study—or ABCD Study—will complete its 2-year enrollment period in September, and this month will release a trove of data from 4500 early participants into a freely accessible, anonymized database. Ultimately, the study aims to follow 10,000 children for a decade as they grow from 9- and 10-year-olds into young adults. Supported by the first chunk of $300 million pledged by several institutes at the National Institutes of Health (NIH) in Bethesda, Maryland, teams at 21 sites around the United States are regularly using MRI machines to record the structure and activity of these young brains. They're also collecting reams of psychological, cognitive, and environmental data about each child, along with biological specimens such as their DNA. In addition to providing the first standardized benchmarks of healthy adolescent brain development, this information should allow scientists to probe how substance use, sports injuries, screen time, sleep habits, and other influences may affect—or be affected by—a maturing brain. © 2017 American Association for the Advancement of Science.

Keyword: Development of the Brain; Schizophrenia
Link ID: 24488 - Posted: 01.04.2018

Amy Maxmen Name a remedy, and chances are that Elizabeth Allen has tried it: acupuncture, antibiotics, antivirals, Chinese herbs, cognitive behavioural therapy and at least two dozen more. She hates dabbling in so many treatments, but does so because she longs for the healthy days of her past. The 34-year-old lawyer was a competitive swimmer at an Ivy-league university when she first fell ill with chronic fatigue syndrome, 14 years ago. Her meticulous records demonstrate that this elusive malady is much worse than ordinary exhaustion. “Last year, I went to 117 doctor appointments and I paid $18,000 in out-of-pocket expenses,” she says. Dumbfounded that physicians knew so little about chronic fatigue syndrome — also known as myalgic encephalomyelitis or ME/CFS — Allen resolved several years ago to take part in any study that would have her. In 2017, she got her chance: she entered a study assessing how women with ME/CFS respond to synthetic hormones. After decades of pleading, people with the condition have finally caught the attention of mainstream science — and dozens of exploratory studies are now under way. Scientists entering the field are using the powerful tools of modern molecular biology to search for any genes, proteins, cells and possible infectious agents involved. They hope the work will yield a laboratory test to diagnose ME/CFS — which might have several different causes and manifestations — and they want to identify molecular pathways to target with drugs. © 2018 Macmillan Publishers Limited,

Keyword: Depression; Neuroimmunology
Link ID: 24487 - Posted: 01.04.2018

By Catherine Offord Graduate student Anne Murphy had run out of rats. Or rather, she’d run out of male rats, the animals she was using to study brain regions involved in pain modulation for her PhD at the University of Cincinnati in the early 1990s. At a time when neuroscientists almost exclusively used male animals for research, what Murphy did next was unusual: she used a female rat instead. “I had the hardest time to get the female to go under the anesthesia; she wasn’t acting right,” Murphy says. Her advisor’s explanation? “‘Well, you know those females, they have hormones, and those hormones are always fluctuating and they’re so variable,’” Murphy recalls. The comments struck a nerve. “It really got to me,” she says. “I’m a female. I have hormones that fluctuate. . . . It made me determined to investigate the differences between males and females in terms of pain processing and alleviation.” Her decision was timely. Since the ’90s, evidence has been accumulating to suggest that not only do women experience a higher incidence of chronic pain syndromes than men do—fibromyalgia and interstitial cystitis, for example—females also generally report higher pain intensities. Additionally, Murphy notes, a handful of clinical studies has suggested that women require higher doses of opioid pain medications such as morphine for comparable analgesia; plus, they experience worse side effects and a higher risk of addiction. © 1986-2018 The Scientist

Keyword: Pain & Touch; Sexual Behavior
Link ID: 24486 - Posted: 01.04.2018

Beyond the usual suspects of snakes, spiders, and scorpions, the animal kingdom is filled with noxious critters: snails, frogs, fish, anemones, and more make toxins for defense or predation. The noxious chemicals these animals produce are potent, and they often strike where it hurts: pain pathways. These compounds have long captivated researchers hoping to understand their effects and use that knowledge to develop drugs that suppress pain in a wide variety of ailments affecting humans. Paradoxically, some of these toxins are themselves analgesic, and researchers have worked to develop synthetic derivatives that can be tested as painkillers. Such is the case for the only toxin-derived analgesic to be approved by the US Food and Drug Administration (FDA): ziconotide (Prialt), a compound 1,000 times more potent than morphine that was inspired by a component of the venom of the cone snail Conus magus. Other toxins elicit pain, and researchers have used these compounds to identify inhibitors of ion channels on the pain-sensing neurons they target. Despite more than half a century of research in this field, however, scientists have had a frustrating time developing effective analgesics. Challenges include ensuring that the drugs are highly specific to their targets—each family of ion channels involved in pain sensing in humans contains several conserved proteins—and getting them to those targets, which often lie beyond the blood-brain barrier in the central nervous system. Nevertheless, several toxin-derived candidates are beginning to prove their worth in preclinical experiments and a handful of clinical trials, and bioprospectors continue to mine the animal kingdom’s vast library of venoms and poisons for more leads. The next big thing in painkillers could soon be slithering, creeping, hopping, or swimming into the pipeline. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24485 - Posted: 01.04.2018

Phil Plait I can't think of a better way to start off a new year than scrambling your brains. Just a little bit! But still: enough to make you scratch your head and wonder just what is wrong with that sack of wrinkly pink goo in your skull. One of my favorite optical illusionists is Akiyoshi Kitaoki. He has created hundreds, maybe thousands, of guaranteed brain-melting illusions that will make you swear that what you're seeing is real when it really, really isn't. He has ones that appear to move, that warp your sense of shape and size, destroy your notion of color, and will make you seriously question whether your eyes and brain are talking to each other in any sort of coherent way. He just posted a new one to Twitter, and I love it for its simplicity and efficiency: It creates two illusions at once. Are you ready? Here it is: I don't know about you, but when I look at this I see alternating squarish shapes (Kitaoka called them turtles, so I'll go with that) arranged like a chessboard, with half darked and half lighter. What's disturbing immediately though is that they don't appear to be separated along straight lines. The vertical border of the turtles on the left appear to curve to the right a bit, and the ones on the right curve left. It makes it look like there's a mound or bulge in the middle of the image.

Keyword: Vision
Link ID: 24484 - Posted: 01.04.2018