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F.D.A. Approves Drug to Treat Pain Without Opioid Effects

By Gina Kolata The Food and Drug Administration approved a new medication Thursday to treat pain from an injury or surgery. It is expensive, with a list price of $15.50 per pill. But unlike opioid pain medicines, it cannot become addictive. That is because the drug, suzetrigine, made by Vertex Pharmaceuticals and to be sold as Journavx, works only on nerves outside the brain, blocking pain signals. It cannot get into the brain. Researchers say they expect it to be the first of a new generation of more powerful nonaddictive drugs to relieve pain. To test the drug, Vertex, which is based in Boston, conducted two large clinical trials, each with approximately 1,000 patients who had pain from surgery. They were randomly assigned to get a placebo; to get the opioid sold as Vicodin, a widely used combination pain medicine of acetaminophen (Tylenol) and hydrocodone; or to get suzetrigine. In one trial, patients had an abdominoplasty, or tummy tuck. In the other, they had a bunionectomy. Side effects of suzetrigine reported by patients were similar to the ones reported by those taking the placebo. The company also submitted data from a 250-person study that assessed the drug’s safety and tolerability in patients with pain from surgery, trauma or accidents. Suzetrigine eased pain as much as the combination opioid. Both were better than the placebo at relieving pain. Suzetrigine’s price, though, is much higher than that of acetaminophen plus hydrocodone. Patients are expected to take two pills a day, for a total cost of $31 a day. The older drug, said Dr. John D. Loeser, an emeritus pain expert at the University of Washington, is “dirt cheap” at pennies per pill. But suzetrigine does not have opioids’ unpleasant side effects like nausea and drowsiness, and it is nonaddictive. © 2025 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 29653 - Posted: 02.01.2025

Scratching an itch is so good, and so bad

By Laura Sanders Scratching an itch can bring a contradictory wave of pleasure and misery. A mouse study on scratching, reported in the Jan. 31 Science, fleshes out this head-scratching paradox and could point out ways to better curb pernicious itch in people. First, the bad news: Scratching itchy ears led to a round of inflammation. Itch-provoking substances, such as the oil in poison ivy, activate mast cells, immune sentries that release itch signals and kick off inflammation. But so does scratching, the new study suggests. “The act of scratching is actually triggering the inflammation by synergizing with mast cells to make them more effective,” says study coauthor Daniel Kaplan, a dermatologist and immunologist at the University of Pittsburgh. Mice that couldn’t scratch their itchy ears, thanks to tiny cones of shame, had less inflammation than mice that scratched. The same was true for mice that didn’t sense the itch, the researchers report. Kaplan relates the results to a mosquito bite. “Most of the time, it’ll go away in five, 10 minutes,” he says. “But if you start scratching it, now, you get a really big, inflamed, itchy lesion on your skin that can stick around for several days. It’s a lot worse. And I think this could be a mechanism that explains why.” Now onto the good news: Scratching lessened the amount of potentially harmful bacteria (Staphylococcus aureus) on mice’s skin, perhaps through the heightened immune reaction it prompts. “That was a clear demonstration that scratching can have a benefit in the context of an acute infection,” Kaplan says. But too much scratching can rip the skin and usher in more bacteria, he cautions. “In that sense, scratching, through a different mechanism, also makes things even worse.” © Society for Science & the Public 2000–2025.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 29648 - Posted: 02.01.2025

Chronic Pain Is a Hidden Epidemic. It’s Time for a Revolution.

By Jennifer Kahn Here’s a strange story: One day two summers ago, I woke up because my arms — both of them — hurt. Not the way they do when you’ve slept in a funny position, but as if the tendons in my forearms and hands were moving through mud. What felt like sharp electric shocks kept sparking in my fingers and sometimes up the inside of my biceps and across my chest. Holding anything was excruciating: a cup, a toothbrush, my phone. Even doing nothing was miserable. It hurt when I sat with my hands in my lap, when I stood, when I lay flat on the bed or on my side. The slightest pressure — a bedsheet, a watch band, a bra strap — was intolerable. It was August, and every doctor seemed to be away on vacation. The ones I did manage to see were politely stumped. It wasn’t carpal tunnel, tennis elbow or any other injury they could identify. I did nothing unusual the day before: an hour of work on my laptop, followed by a visit with a friend. We sat in her backyard and talked. For the first few weeks, I could barely sleep. Over the following months, I lost weight — almost a pound a week. I couldn’t drive, or cook, or use my laptop for work, or even hold a book or a pen. I would have been bored, except the pain was so tiring that I could barely function. I spent the days shuffling around the house listening to audiobooks and doing voice-to-text searches for “nerve pain arms” with my phone flat on the table, then carefully, painfully, scrolling through the results. I think we’re past the point where I have to explain that chronic pain is not the result of imbalanced humors or a wandering uterus or possession by demons. But for more modern skeptics, this is where I should add that chronic pain also isn’t just “all in your head” or “not really that bad” — or any of the other ways in which people who suffer from it are still regularly gaslit and dismissed. Personally, I never had to contend with not being believed, almost certainly because I’m an otherwise healthy, reasonably well-off white woman with a clean medical history and no significant record of anxiety or depression. Instead, I was taken seriously. A whole gamut of tests was run. My wrists were X-rayed. I had an M.R.I. on my cervical spine. Each new doctor ordered new blood tests: some for vitamin deficiencies, others for autoimmune diseases like rheumatoid arthritis. © 2025 The New York Times Company

She Was Scratching Her Arms Raw. Would Anything Stop This Itch?

By Lisa Sanders, M.D. The 62-year-old woman shifted in her seat. The flight to Honolulu was full, the mood a little giddy. The unbroken ocean and sky filled the window. She and her daughter were four hours into the trip from Los Angeles to the wedding of a close family friend; it was going to be a great week. Then, she caught herself scratching lightly at a place on her forearm, just below the crease of her elbow. She lifted her arm to look at the spot. Nothing there. Immediately she was filled with dread. She reached over her head to touch the call button. She needed ice, lots of ice, and she needed it right away. The mild itch had already exploded into spasms of an intense sensation — it seemed wrong to call it an itch; surely there was a better word for it. The fierce intensity of the feeling shocked her. It was a feeling that insisted she scratch. Except scratching never helped. And she had the scars to prove it. She had suffered episodes of itching like this a few times in the past couple of years, though never quite as bad as it was on this flight. Her doctor back home had no idea what caused the crazy itch or what more she might do about it. These attacks came out of nowhere but immediately brought life to a standstill as she tried to ease the unbearable sensation. A bout could last for hours and almost always ended with her arm a bloody mess. When her daughter first saw her mother raking her nails over the invisible injury and the distress she felt fighting this unwinnable battle, she had offered her a Valium. And it helped. The itch was still there but the intensity somehow lessened. On the flight, the woman retrieved the pills she now carried with her all the time. The little bags of ice brought by the flight attendant melted slowly, numbing the hand that pressed them against her arm and easing the itch. She knew from experience that as soon as the ice was removed, the itch would roar back. The attendant brought an ice bucket. But within the hour, she needed more ice. More Valium. She was drenched with the condensation. Her clothes were dotted with blood. She didn’t care. She just had to get through it. © 2024 The New York Times Company

Opioid-free surgery treats pain at every physical and emotional level

Heather Margonari The opioid crisis remains a significant public health challenge in the United States. In 2022, over 2.5 million American adults had an opioid use disorder, and opioids accounted for nearly 76% of overdose deaths. Some patients are fearful of using opioids after surgery due to concerns about dependence and potential side effects, even when appropriately prescribed by a doctor to manage pain. Surgery is often the first time patients receive an opioid prescription, and their widespread use raises concerns about patients becoming long-term users. Leftover pills from a patient’s prescriptions may also be misused. Researchers like us are working to develop a personalized and comprehensive surgical experience that doesn’t use opioids. Our approach to opioid-free surgery addresses both physical and emotional well-being through effective anesthesia and complementary pain-management techniques. What is opioid-free anesthesia? Clinicians have used morphine and other opioids to manage pain for thousands of years. These drugs remain integral to anesthesia. Help us raise up the voices of experts. Most surgical procedures use a strategy called balanced anesthesia, which combines drugs that induce sleep and relax muscles with opioids to control pain. However, using opioids in anesthesia can lead to unwanted side effects, such as serious cardiac and respiratory problems, nausea and vomiting, and digestive issues. Concerns over these adverse effects and the opioid crisis have fueled the development of opioid-free anesthesia. This approach uses non-opioid drugs to relieve pain before, during and after surgery while minimizing the risk of side effects and dependency. Studies have shown that opioid-free anesthesia can provide similar levels of pain relief to traditional methods using opioids. Copyright © 2010–2024, The Conversation US, Inc.

Chronic itch is miserable. Scientists are just scratching the surface

Terry Gross We've all had bug bites, or dry scalp, or a sunburn that causes itch. But what if you felt itchy all the time — and there was no relief? Journalist Annie Lowrey suffers from primary biliary cholangitis (PBC), a degenerative liver disease in which the body mistakenly attacks cells lining the bile ducts, causing them to inflame. The result is a severe itch that doesn't respond to antihistamines or steroids. "It feels like being trapped inside your own body," Lowrey says of the disease. "I always describe it as being like a car alarm. Like, you can't stop thinking about it." PBC is impacts approximately 80,000 people in the U.S., the majority of whom are women. At its worst, Lowrey says, the itch caused her to dig holes in her skin and scalp. She's even fantasized about having limbs amputated to escape the itch. Lowrey writes about living with PBC in the Atlantic article, "Why People Itch and How to Stop It." She says a big part of her struggle is coming to terms with the fact that she may never feel fully at ease in her skin. "I talked to two folks who are a lot older than I was, just about like, how do you deal with it? How do you deal with the fact that you might itch and never stop itching? … And both of them were kind of like, 'You put up with it, stop worrying about it and get on with your life,'" she says. "I think I was mentally trapped ... and sometimes it's like, OK, ... go do something else. Life continues on. You have a body. It's OK." © 2024 npr

Why do wet dogs shake themselves dry? Neuroscience has an answer

By Miryam Naddaf When a dog shakes water off its fur, the action is not just a random flurry of movements — nor a deliberate effort to drench anyone standing nearby. This instinctive reflex is shared by many furry mammals including mice, cats, squirrels, lions, tigers and bears. The move helps animals to remove water, insects or other irritants from hard-to-reach places. But underlying the shakes is a complex — and previously mysterious — neurological mechanism. Now, researchers have identified the neural circuit that triggers characteristic ‘wet dog’ shaking behaviour in mice — which involves a specific class of touch receptors, and neurons that connect the spinal cord to the brain. Their findings were published in Science on 7 November1. “The touch system is so complex and rich that [it] can distinguish a water droplet from a crawling insect from the gentle touch of a loved one,” says Kara Marshall, a neuroscientist at Baylor College of Medicine in Houston, Texas. “It’s really remarkable to be able to link a very specific subset of touch receptors to this familiar and understandable behaviour.” The hairy skin of mammals is packed with more than 12 types of sensory neuron, each with a unique function to detect and interpret various sensations. Study co-author Dawei Zhang, a neuroscientist then at Harvard Medical School in Boston, Massachusetts, and his colleagues focused on a type of ultra-sensitive touch detecting receptors called C-fibre low-threshold mechanoreceptors (C-LTMRs), which wrap around hair follicles. In humans, these receptors are associated with pleasant touch sensations, such as a soft hug or a soothing stroke. But in mice and other animals, they serve a protective role: alerting them to the presence of something on their skin, whether it’s water, dirt or a parasite. When these stimuli cause hairs on the skin to bend it activates the C-LTMRs, says Marshall, “extending the sensibility of the skin beyond just the surface”. © 2024 Springer Nature Limited

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 29551 - Posted: 11.09.2024

Studies of migraine’s many triggers offer paths to new therapies

By Amber Dance For Cherise Irons, chocolate, red wine and aged cheeses are dangerous. So are certain sounds, perfumes and other strong scents, cold weather and thunderstorms. Stress and lack of sleep, too. She suspects all of these things can trigger her migraine attacks, which manifest in a variety of ways: pounding pain in the back of her head, exquisite sensitivity to the slightest sound, even blackouts and partial paralysis. Irons, 48, of Coral Springs, Florida, once worked as a school assistant principal. Now, she’s on disability due to her migraine. Irons has tried so many migraine medications she’s lost count — but none has helped for long. Even a few of the much-touted new drugs that have quelled episodes for many people with migraine have failed for Irons. Though not all are as impaired as Irons, migraine is a surprisingly common problem, affecting 14 percent to 15 percent of people. Yet scientists and physicians remain largely in the dark about how triggers like Irons’s lead to attacks. They have made progress nonetheless: The latest drugs, inhibitors of a body signaling molecule called CGRP, have been a blessing for many. For others, not so much. And it’s not clear why. The complexity of migraine probably has something to do with it. “It’s a very diverse condition,” says Debbie Hay, a pharmacologist at the University of Otago in Dunedin, New Zealand. “There’s still huge debate as to what the causes are, what the consequences are.”

Hair pulling prompts one of the fastest known pain signals

By Laura Sanders CHICAGO — Big news for fighting sisters: Scientists have found the sensors that signal the painful zing of a hair pull. And this pain message can rip along a nerve fiber at about 100 miles an hour, placing it among the fastest known pain signals. The discovery, presented October 8 at the annual meeting of the Society for Neuroscience, offers insight into the diverse ways our bodies sense and respond to different sorts of pain. Pain can come from many catastrophes — cuts, jabs, pinches, cramps, bites, slaps, stubbing a toe in the dark. And while our bodies can generally tell these insults apart thanks to a variety of biological pathways, they all hurt. “It’s not surprising that we have figured out many, many ways to make [pain] happen,” says neuroscientist Gregory Dussor of the University of Texas at Dallas. “Because when it doesn’t, we don’t live.” Laboratory tests showed a hair pull to be about 10 times as painful as a pinprick, neuroscientist Emma Kindström of Linköping University in Sweden and colleagues found. The pain of the pull relies on a large, propeller-shaped protein called PIEZO2, further tests showed. That sensor was known to detect mechanical forces, including light touches, but wasn’t thought to detect acute pain signals. People who lack this protein don’t feel hair-pull pain. A hair-pull signal moves along nerve fibers much faster than other sorts of pain, Kindström says, traveling in bursts along an insulated conduit called an Aβ nerve fiber. Other kinds of pain signals, such as a burn from a hot stove, travel more slowly along different kinds of fibers. © Society for Science & the Public 2000–2024.

A next-gen pain drug shows promise, but chronic sufferers need more options

By Cassandra Willyard Megan Hodge’s first bout of intense pain arrived when she was in her mid-20s. Hodge and her husband were getting ready to visit family for Thanksgiving. Though Hodge had been dealing with a variety of chronic health issues, her workout had gone well that morning and she finally felt like she was getting a handle on her health. Hodge began packing. As she reached into her closet to grab a sweater, her back gave out. The pain was excruciating, so intense that she felt light-headed and thought she might vomit. As the years passed, Hodge had more frequent and more severe bouts of back pain. Any small movement could be a trigger — grabbing a towel from the linen closet, picking up a toy off the floor, sneezing. In 2021, Hodge experienced a particularly bad flare-up. None of the strategies she had previously used to help her manage seemed to be working. She was afraid to make any movement. She felt hopeless. “I just could not regain footing, metaphorically and physically,” she says. “I truly felt frozen in my chronic pain and chronic health journey.” Hodge is far from alone. In the United States, chronic pain affects tens of millions of people — about 1 in 5 adults and nearly 1 in 3 people ages 65 and older. “The amount of suffering from arthritis and aging that I’ve seen in my pain clinic, it’s overwhelming to me as a pain doctor,” says Antje Barreveld, an anesthesiologist at Mass General Brigham’s Newton-Wellesley Hospital in Massachusetts. What’s more, the mainstay therapy for severe acute and chronic pain — prescription opioids — has helped fuel an epidemic that kills tens of thousands of people each year. “We have to have some better alternatives,” she says. So researchers have doubled down in their quest to find new pain treatments that aren’t as addictive as opioids. “The pain field has really made very rapid and tremendous progress in the last decade,” says D.P. Mohapatra, a former pain scientist who now oversees research at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. © Society for Science & the Public 2000–2024.

New Pain Medication Suzetrigine Prevents Pain Signals from Reaching Brain

By Marla Broadfoot When doctors ask Sara Gehrig to describe her pain, she often says it is indescribable. Stabbing, burning, aching—those words frequently fail to depict sensations that have persisted for so long they are now a part of her, like her bones and skin. “My pain is like an extra limb that comes along with me every day.” Gehrig, a former yoga instructor and personal trainer who lives in Wisconsin, is 44 years old. At the age of 17 she discovered she had spinal stenosis, a narrowing of the spinal cord that puts pressure on the nerves there. She experienced bursts of excruciating pain in her back and buttocks and running down her legs. That pain has spread over the years, despite attempts to fend it off with physical therapy, anti-inflammatory injections and multiple surgeries. Over-the-counter medications such as ibuprofen (Advil) provide little relief. And she is allergic to the most potent painkillers—prescription opioids—which can induce violent vomiting. Today her agony typically hovers at a 7 out of 10 on the standard numerical scale used to rate pain, where 0 is no pain and 10 is the most severe imaginable. Occasionally her pain flares to a 9 or 10. At one point, before her doctor convinced her to take antidepressants, Gehrig struggled with thoughts of suicide. “For many with chronic pain, it’s always in their back pocket,” she says. “It’s not that we want to die. We want the pain to go away.” Gehrig says she would be willing to try another type of painkiller, but only if she knew it was safe. She keeps up with the latest research, so she was interested to hear earlier this year that Vertex Pharmaceuticals was testing a new drug that works differently than opioids and other pain medications. That drug, a pill called VX-548, blocks pain signals before they can reach the brain. It gums up sodium channels in peripheral nerve cells, and obstructed channels make it hard for those cells to transmit pain sensations. Because the drug acts only on the peripheral nerves, it does not carry the potential for addiction associated with opioids—oxycodone (OxyContin) and similar drugs exert their effects on the brain and spinal cord and thus can trigger the brain’s reward centers and an addiction cycle.

The Painkiller Used for Just About Anything

By Paula Span Mary Peart, 67, a retired nurse in Manchester-by-the-Sea, Mass., began taking gabapentin a year and a half ago to reduce the pain and fatigue of fibromyalgia. The drug helps her climb stairs, walk her dog and take art lessons, she said. With it, “I have a life,” she said. “If I forget to take a dose, my pain comes right back.” Jane Dausch has a neurological condition called transverse myelitis and uses gabapentin as needed when her legs and feet ache. “It seems to be effective at calming down nerve pain,” said Ms. Dausch, 67, a retired physical therapist in North Kingstown, R.I. Amy Thomas, who owns three bookstores in the San Francisco Bay Area, takes gabapentin for rheumatoid arthritis. Along with yoga and physical therapy, “it’s probably contributing to it being easier for me to move around,” Ms. Thomas, 67, said. All three are taking the non-opioid pain drug for off-label uses. The only conditions for which gabapentin has been approved for adult use by the Food and Drug Administration are epileptic seizures, in 1993, and postherpetic neuralgia, the nerve pain that can linger after a bout of shingles, in 2002. But that has not stopped patients and health care providers from turning to gabapentin (whose brand names include Neurontin) for a startling array of other conditions, including sciatica, neuropathy from diabetes, lower back pain and post-surgery pain. Also: Agitation from dementia. Insomnia. Migraines. Itching. Bipolar disorder. Alcohol dependence. Evidence of effectiveness for these conditions is all over the map. The drug appears to provide relief for some patients with diabetic neuropathy but not with some other kinds of neuropathic pain. Several small studies indicate that gabapentin can reduce the itching associated with kidney failure. But the data for its effectiveness against low back pain or a number of psychiatric disorders are limited and show no meaningful impact. “It’s crazy how many indications it’s used for,” said Dr. Michael Steinman, a geriatrician at the University of California, San Francisco, and a co-director of the U.S. Deprescribing Research Network. “It’s become a we-don’t-know-what-else-to-do drug.” © 2024 The New York Times Company

What causes migraines? Study of ‘brain blackout’ offers clues

By Miryam Naddaf About one-third of people who suffer from migraines experience a phenomenon known as aura before the headache.Credit: Tunatura/Getty For one billion people worldwide, the symptoms can be debilitating: throbbing head pain, nausea, blurred vision and fatigue that can last for days. But how brain activity triggers these severest of headaches — migraines — has long puzzled scientists. A study1 in mice, published in Science on 4 July, now offers clues about the neurological events that spark migraines. It suggests that a brief brain ‘blackout’ — when neuronal activity shuts down — temporarily changes the content of the cerebrospinal fluid, the clear liquid that surrounds the brain and spinal cord. This altered fluid, researchers suggest, travels through a previously unknown gap in anatomy to nerves in the skull where it activates pain and inflammatory receptors, causing headaches. “This work is a shift in how we think the headaches originate,” says Gregory Dussor, a neuroscientist at the University of Texas at Dallas in Richardson. “A headache might just be a general warning sign for lots of things happening inside the brain that aren’t normal.” “Migraine is actually protective in that way. The pain is protective because it’s telling the person to rest and recover and sleep,” says study co-author Maiken Nedergaard, a neuroscientist at the University of Copenhagen. The brain itself has no pain receptors; the sensation of headaches comes from areas outside the brain that are in the peripheral nervous system. But how the brain, which is not directly linked to the peripheral nervous system, triggers nerves to cause headaches is poorly understood, making them difficult to treat. © 2024 Springer Nature Limited

How does a migraine aura trigger a headache?

By Rodrigo Pérez Ortega It starts with blind spots, flashing lights, and blurry vision—a warning of what’s to come. About an hour later, the dreadful headache kicks in. This pairing, a shining visual experience called an aura and then a headache, happens in about one-third of people who live with migraine. But researchers haven’t been able to figure out exactly how the two are linked at the molecular level. Now, a new study in mice, published today in Science, establishes a direct mechanism: molecules traveling in the fluid that bathes the brain. The finding could lead to new targets for much-needed migraine treatments. “It’s exciting,” says Rami Burstein, a translational neuroscientist at Harvard Medical School who was not involved in the new study. “It takes a very large step into understanding how something that happened in the brain can alter sensation or perception,” he says. It may also explain why the pain of migraine is experienced only in the head, he adds. Migraine, a debilitating neurological disorder, affects about 148 million people worldwide. Recently developed medications can help reduce headaches but are not effective for everyone. Although exact causes remain elusive, research has shown migraines most likely start with a pathological burst of neural activity. During an aura before a migraine, researchers have observed a seizurelike phenomenon called cortical spreading depression (CSD), in which a wave of abnormal neural firing slowly travels throughout the brain’s outer layer, or cortex. But because the brain itself contains no pain-sensing neurons, signals from the brain would have to somehow reach the peripheral nervous system—the nerves that communicate between the body parts and the brain—to cause a headache. In particular, they’d have to get to the two lumps of neurons below the brain called the trigeminal ganglia, which innervate the two sides of our face and head. Scientists knew that pain fibers from the trigeminal ganglion were nested in the meninges—the thin, delicate membranes that envelop and protect the brain.

Pain may take different pathways in men and women

By Claire Yuan Men and women experience pain differently, and until now, scientists didn’t know why. New research says it may be in part due to differences in male and female nerve cells. Pain-sensing nerve cells from male and female animal tissues responded differently to the same sensitizing substances, researchers report June 3 in Brain. The results suggest that at the cellular level, pain is produced differently between the sexes. The results might allow researchers “to come up with drugs that would be specific to treat female patients or male patients,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine and was not involved in the study. “There’s no debate about it. They’re seeing these differences in the cells.” Some types of chronic and acute pain appear more often in one sex, but it’s unclear why. For instance, about 50 million adults in the United States suffer from chronic pain conditions, many of which are more common in women (SN: 5/22/23). Similar disparities exist for acute conditions. Such differences prompted pain researcher Frank Porreca of the University of Arizona Health Sciences in Tucson and colleagues to study nerve cells called nociceptors, which can act like alarm sensors for the body. The cells’ pain sensors, found in skin, organs and elsewhere in the body, can detect potentially dangerous stimuli and send signals to the brain, which then interprets the information as pain. In some cases, the nerve cells can become more sensitive to outside stimulation, registering even gentle sensations — like a shirt rubbing sunburned skin — as pain. © Society for Science & the Public 2000–2024.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 29366 - Posted: 06.24.2024

Pleasure or Pain? He Maps the Neural Circuits That Decide.

By Ingrid Wickelgren Ishmail Abdus-Saboor has been fascinated by the variety of the natural world since he was a boy growing up in Philadelphia. The nature walks he took under the tutelage of his third grade teacher, Mr. Moore, entranced him. “We got to interact and engage with wildlife and see animals in their native environment,” he recalled. Abdus-Saboor also brought a menagerie of creatures — cats, dogs, lizards, snakes and turtles — into his three-story home, and saved up his allowance to buy a magazine that taught him about turtles. When adults asked him what he wanted to be when he grew up, “I said I wanted to become a scientist,” he said. “I always raised eyebrows.” Abdus-Saboor did not stray from that goal. Today, he is an associate professor of biological sciences at the Mortimer B. Zuckerman Mind Brain Behavior Institute at Columbia University, where he studies how the brain determines whether a touch to the skin is painful or pleasurable. “Although this question is fundamental to the human experience, it remains puzzling to explain with satisfying molecular detail,” he said. Because the skin is our largest sensory organ and a major conduit to our environment, it may hold clues for treating conditions from chronic pain to depression. To find those clues, Abdus-Saboor probes the nervous system at every juncture along the skin-to-brain axis. He does not focus on skin alone or home in on only the brain as many others do. “We merge these two worlds,” he said. That approach, he added, requires mastering two sets of techniques, reading two sets of literature and attending two sets of scientific meetings. “It gives us a unique leg up,” he said. It has led to a landmark paper published last year in Cell that laid out the entire neural circuit for pleasurable touch. © 2024 Simons Foundation.

Large Scientific Review Confirms the Benefits of Physical Touch

By Joanne Silberner A hug, a handshake, a therapeutic massage. A newborn lying on a mother’s bare chest. Physical touch can buoy well-being and lessen pain, depression and anxiety, according to a large new analysis of published research released on Monday in the journal Nature Human Behaviour. Researchers from Germany and the Netherlands systematically reviewed years of research on touch, strokes, hugs and rubs. They also combined data from 137 studies, which included nearly 13,000 adults, children and infants. Each study compared individuals who had been physically touched in some way over the course of an experiment — or had touched an object like a fuzzy stuffed toy — to similar individuals who had not. For example, one study showed that daily 20-minute gentle massages for six weeks in older people with dementia decreased aggressiveness and reduced the levels of a stress marker in the blood. Another found that massages boosted the mood of breast cancer patients. One study even showed that healthy young adults who caressed a robotic baby seal were happier, and felt less pain from a mild heat stimulus, than those who read an article about an astronomer. Positive effects were particularly noticeable in premature babies, who “massively improve” with skin-to-skin contact, said Frédéric Michon, a researcher at the Netherlands Institute for Neuroscience and one of the study’s authors. “There have been a lot of claims that touch is good, touch is healthy, touch is something that we all need,” said Rebecca Boehme, a neuroscientist at Linkoping University in Sweden, who reviewed the study for the journal. “But actually, nobody had looked at it from this broad, bird’s eye perspective.” © 2024 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 29252 - Posted: 04.11.2024

Sensor protein explains how mice—and maybe people—know it’s cold

By Alejandra Manjarrez People wear gloves when making a snowman for a reason: Handling cold stuff can hurt. A new mouse study reveals what may be a key player in this response: a protein already known to enable sensory neurons in worms to detect cold. New evidence published this week in Nature Neuroscience confirms that this protein has the same function in mammals. “The paper is exciting,” says Theanne Griffith, a neuroscientist at the University of California, Davis who was not involved in the research. She notes that the protein, called GluK2, is found in the brain and has “traditionally been thought to play a major role in learning and memory.” The new work shows that elsewhere in the body, it has an unsuspected and “completely divergent role.” We perceive touch, pain, and temperature thanks to a system of nerves that extends throughout our bodies. Researchers have identified skin sensors that detect hot and warm stimuli. Cold sensors, though, have proved more challenging to find. Researchers have proposed various candidates but found limited and contradictory evidence for their function. An ion channel named TRPM8 is the exception. Famous for detecting the “cool” sensation of menthol, it also detects cold temperatures and helped earn its discoverers the Nobel Prize in Physiology or Medicine in 2021. “Nobody questions that TRPM8 is a cold sensor,” says sensory neurobiologist Félix Viana of the Institute for Neuroscience in Alicante, Spain. But it could not be the whole story. It works most efficiently at temperatures above roughly 10°C, and mice lacking the gene for TRPM8 can still detect very cold temperatures. A few years ago, University of Michigan neuroscientists Shawn Xu and Bo Duan and their colleagues found another candidate: a protein on certain sensory neurons in the tiny roundworm Caenorhabditis elegans that causes the animals to avoid temperatures between 17°C and 18°C, which are colder than their preferred temperatures. Preliminary data from that study hinted that the equivalent protein in mammals, GluK2, also allowed mice to sense cold.

The "shocking" tactic electric fish use to collectively sense the world

By Regina G. Barber, Anil Oza, Ailsa Chang, Rachel Carlson Neuroscientist Nathan Sawtell has spent a lot of time studying a funky looking electric fish characterized by its long nose. The Gnathonemus petersii, or elephantnose fish, can send and decipher weak electric signals, which Sawtell hopes will help neuroscientists better understand how the brain pieces together information about the outside world. But as Sawtell studied these electric critters, he noticed a pattern he couldn't explain: the fish tend to organize themselves in a particular orientation. "There would be a group of subordinates in a particular configuration at one end of the tank, and then a dominant fish at the other end. The dominant fish would swim in and break up the group, and they would scatter. A few seconds later, the group would coalesce and it would stay there for hours at a time in this stationary configuration," Sawtell, who runs a lab at Columbia University's Zuckerman Institute says. Initially Sawtell and his team couldn't put together why the fish were always hanging out in this configuration. "What could they really be talking to each other about all of this time?" A new study released this week in Nature by Sawtell and colleagues at Columbia University could have one potential answer: the fish are creating an electrical network that is larger than any field an individual fish can muster alone. In this collective field, the whole school of fish get instantaneous information on changes in the water around them, like approaching predators. Rather than being confused by the flurry of electric signals from other fish, "these fish were clever enough to exploit the pulses of group members to sense their environment," Sawtell says. © 2024 npr

A new device let a man sense temperature with his prosthetic hand

By Simon Makin A new device makes it possible for a person with an amputation to sense temperature with a prosthetic hand. The technology is a step toward prosthetic limbs that restore a full range of senses, improving both their usefulness and acceptance by those who wear them. A team of researchers in Italy and Switzerland attached the device, called ”MiniTouch,” to the prosthetic hand of a 57-year-old man named Fabrizio, who has an above-the-wrist amputation. In tests, the man could identify cold, cool and hot bottles of liquid with perfect accuracy; tell the difference between plastic, glass and copper significantly better than chance; and sort steel blocks by temperature with around 75 percent accuracy, researchers report February 9 in Med. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. “It’s important to incorporate these technologies in a way that prosthesis users can actually use to perform functional tasks,” says neuroengineer Luke Osborn of Johns Hopkins University Applied Physics Laboratory in Laurel, Md., who was not involved in the study. “Introducing new sensory feedback modalities could help give users more functionality they weren’t able to achieve before.” The device also improved Fabrizio’s ability to tell whether he was touching an artificial or human arm. His accuracy was 80 percent with the device turned on, compared with 60 percent with it off. “It’s not quite as good as with the intact hand, probably because we’re not giving [information about] skin textures,” says neuroengineer Solaiman Shokur of EPFL, the Swiss Federal Institute of Technology in Lausanne. © Society for Science & the Public 2000–2024.

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