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R. Douglas Fields Neuroscientists, being interested in how brains work, naturally focus on neurons, the cells that can convey elements of sense and thought to each other via electrical impulses. But equally worthy of study is a substance that’s between them — a viscous coating on the outside of these neurons. Roughly equivalent to the cartilage in our noses and joints, the stuff clings like a fishing net to some of our neurons, inspiring the name perineuronal nets (PNNs). They’re composed of long chains of sugar molecules attached to a protein scaffolding, and they hold neurons in place, preventing them from sprouting and making new connections. Given this ability, this little-known neural coating provides answers to some of the most puzzling questions about the brain: Why do young brains absorb new information so easily? Why are the fearful memories that accompany post-traumatic stress disorder (PTSD) so difficult to forget? Why is it so hard to stop drinking after becoming dependent on alcohol? And according to new research from the neuroscientist Arkady Khoutorsky and his colleagues at McGill University, we now know that PNNs also explain why pain can develop and persist so long after a nerve injury. Neural plasticity is the ability of neural networks to change in response to experiences in life or to repair themselves after brain injury. Such opportunities for effortless change are known as critical periods when they occur early in life. Consider how easily babies pick up language, but how difficult it is to learn a foreign language as an adult. In a way, this is what we’d want: After the intricate neural networks that allow us to understand our native language are formed, it’s important for them to be locked down, so the networks remain relatively undisturbed for the rest of our lives. All Rights Reserved © 2022

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28415 - Posted: 07.30.2022

ByVirginia Morell We swat bees to avoid painful stings, but do they feel the pain we inflict? A new study suggests they do, a possible clue that they and other insects have sentience—the ability to be aware of their feelings. “It’s an impressive piece of work” with important implications, says Jonathan Birch, a philosopher and expert on animal sentience at the London School of Economics who was not involved with the paper. If the study holds up, he says, “the world contains far more sentient beings than we ever realized.” Previous research has shown honey bees and bumble bees are intelligent, innovative, creatures. They understand the concept of zero, can do simple math, and distinguish among human faces (and probably bee faces, too). They’re usually optimistic when successfully foraging, but can become depressed if momentarily trapped by a predatory spider. Even when a bee escapes a spider, “her demeanor changes; for days after, she’s scared of every flower,” says Lars Chittka, a cognitive scientist at Queen Mary University of London whose lab carried out that study as well as the new research. “They were experiencing an emotional state.” To find out whether these emotions include pain, Chittka and colleagues looked at one of the criteria commonly used for defining pain in animals: “motivational trade-offs.” People will endure the pain of a dentist’s drill for the longer term benefits of healthy teeth, for example. Similarly, hermit crabs will leave preferred shells to escape an electric shock only when given a particularly high jolt—an experiment that demonstrated crabs can tell the difference between weak and strong painful stimuli, and decide how much pain is worth enduring. That suggests crabs do feel pain and don’t simply respond reflexively to an unpleasant stimulus. Partly as a result of that study, crabs (and other crustaceans, including lobsters and crayfish) are recognized as sentient under U.K. law. © 2022 American Association for the Advancement of Science

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: 28410 - Posted: 07.30.2022

By Meghan Rosen A flexible electronic implant could one day make pain management a lot more chill. Created from materials that dissolve in the body, the device encircles nerves with an evaporative cooler. Implanted in rats, the cooler blocked pain signals from zipping up to the brain, bioengineer John Rogers and colleagues report in the July 1 Science. Though far from ready for human use, a future version could potentially let “patients dial up or down the pain relief they need at any given moment,” says Rogers, of Northwestern University in Evanston, Ill. Scientists already knew that low temperatures can numb nerves in the body. Think of frozen fingers in the winter, Rogers says. But mimicking this phenomenon with an electronic implant isn’t easy. Nerves are fragile, so scientists need something that gently hugs the tissues. And an ideal implant would be absorbed by the body, so doctors wouldn’t have to remove it. Made from water-soluble materials, the team’s device features a soft cuff that wraps around a nerve like toilet paper on a roll. Tiny channels snake down its rubbery length. When liquid coolant that’s pumped through the channels evaporates, the process draws heat from the underlying nerve. A temperature sensor helps scientists hit the sweet spot — cold enough to block pain but not too cold to damage the nerve. The researchers wrapped the implant around a nerve in rats and tested how they responded to having a paw poked. With the nerve cooler switched on, scientists could apply about seven times as much pressure as usual before the animals pulled their paws away. That’s a sign that the rats’ senses had grown sluggish, Rogers says. © Society for Science & the Public 2000–2022.

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: 28387 - Posted: 07.05.2022

Sofia Quaglia When they are in the deep, dark ocean, seals use their whiskers to track down their prey, a study has confirmed after observing the sea mammals in their natural habitat. It’s hard for light to penetrate the gloom of the ocean’s depths, and animals have come up with a variety of adaptations in order to live and hunt there. Whales and dolphins, for example, use echolocation – the art of sending out clicky noises into the water and listening to their echo as they bounce off possible prey, to locate them. But deep-diving seals who don’t have those same acoustic projectors must have evolutionarily learned to deploy another sensory technique. Scientists have long hypothesised that the secret weapons are their long, cat-like whiskers, conducting over 20 years of experiments with artificial whiskers or captive seals blindfolded in a pool, given the difficulties of directly observing the hunters in the tenebrous depths of the ocean. Now a study may have confirmed the hypothesis, according to Taiki Adachi, assistant project scientist of University of California, Santa Cruz, and one of the lead authors of the study published in Proceedings of the National Academy of Science. Adachi and his team positioned small video cameras with infrared night-vision on the left cheek, lower jaw, back and head of five free-ranging northern elephant seals, the Mirounga angustirostris, in Año Nuevo state park in California. They recorded a total of approximately nine and a half hours of deep sea footage during their seasonal migration. By analysing the videos the scientists noted that diving seals held back their whiskers for the initial part of their dives and, and once they reached a depth suitable for foraging, they rhythmically whisked their whiskers back and forth, hoping to sense any vibration caused by the slightest water movements of swimming prey. © 2022 Guardian News & Media Limited o

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: 28368 - Posted: 06.14.2022

By Maria Temming The Terminator may be one step closer to reality. Researchers at the University of Tokyo have built a robotic finger that, much like Arnold Schwarzenegger’s titular cyborg assassin, is covered in living human skin. The goal is to someday build robots that look like real people — albeit for more altruistic applications. Super realistic-looking robots could more seamlessly interact with humans in medical care and service industries, say biohybrid engineer Shoji Takeuchi and his colleagues June 9 in Matter. (Whether cyborgs masked in living tissue would be more congenial or creepy is probably in the eye of the beholder.) To cover the finger in skin, Takeuchi and colleagues submerged the robotic digit in a blend of collagen and human skin cells called dermal fibroblasts. The mixture settled into a base layer of skin, or dermis, covering the finger. The team then poured a liquid containing human keratinocyte cells onto the finger, which formed an outer skin layer, or epidermis. After two weeks, skin covering the finger measured a few millimeters thick — comparable to the thickness of human skin. The lab-made skin was strong and stretchy enough to withstand the robotic finger bending. It could also heal itself: When researchers made a small cut on the robotic finger and covered it with a collagen bandage, the skin’s fibroblast cells merged the bandage with the rest of the skin within a week. Researchers at the University of Tokyo covered this robotic finger in living human skin to pave the way for ultrarealistic cyborgs. “This is very interesting work and an important step forward in the field,” says Ritu Raman, an MIT engineer who also builds machines with living components. “Biological materials are appealing because they can dynamically sense and adapt to their environments.” For instance, she’d like to see a future version of the living robot skin embedded with nerve cells to make robots more aware of their surroundings. © Society for Science & the Public 2000–2022.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 28365 - Posted: 06.11.2022

By Gina Kolata The very treatments often used to soothe pain in the lower back, which the Centers for Disease Control and Prevention says is the most common type of pain, might cause it to last longer, according to a new study. Managing pain with steroids and nonsteroidal anti-inflammatory drugs, like ibuprofen, can actually turn a wrenched back into a chronic condition, the study found. Some medical experts urged caution in interpreting the results too broadly. The study did not use the gold standard for medical research, which would be a clinical trial in which people with back pain would be randomly assigned to take a nonsteroidal anti-inflammatory drug or a placebo and followed to see who developed chronic pain. Instead, it involved observations of patients, an animal study and an analysis of patients in a large database. “It’s intriguing but requires further study,” said Dr. Steven J. Atlas, director of primary care practice-based research and quality improvement at Massachusetts General Hospital. Dr. Bruce M. Vrooman, a pain specialist at Dartmouth Hitchcock Medical Center in New Hampshire, agreed, but also called the study “impressive in its scope” and said that if the results hold up in a clinical trial, it could “force reconsideration of how we treat acute pain.” Dr. Thomas Buchheit, director of the regenerative pain therapies program at Duke, had a different view. “People overuse the term ‘paradigm shift’, but this is absolutely a paradigm shift,” Dr. Buchheit said. “There is this unspoken rule: If it hurts, take an anti-inflammatory, and if it still hurts, put a steroid on it,” he added. “But,” he said, the study shows that “we have to think of healing and not suppression of inflammation.” Guidelines from professional medical societies already say that people with back pain should start with nondrug treatments like exercise, physical therapy, heat or massage. Those measures turn out to be as effective as pain-suppressing drugs, without the same side effects. © 2022 The New York Times Company

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: 28328 - Posted: 05.18.2022

Perspective by Susan Berger As I faced a prophylactic double mastectomy in hopes of averting cancer, I had many questions for my surgeons — one of which was about pain. I was stunned when both my breast surgeon and plastic surgeon said that a nerve block would leave me pain-free for about three days, after which the worst of the pain would be over. Pectoralis nerve (PECS) blocks were developed to provide analgesia or pain relief for chest surgeries, including breast surgery. That is what happened. I went through the mastectomy Dec. 1 after learning I had the PALB2 gene mutation that carried a sharply elevated risk of breast cancer as well as a higher risk of ovarian and pancreatic cancers. I also had my fallopian tubes and ovaries removed in July. I had learned about the gene mutation in April 2021, when one of my daughters found out she was a carrier. As a 24-year breast cancer survivor and longtime health reporter, I was astonished that I had heard nothing about this mutation. I researched it and wrote “This Breast Cancer Gene Is Less Well Known, but Nearly as Dangerous” in August. After the double mastectomy, I also wrote about it for The Washington Post. Just as my surgeons at NorthShore University HealthSystem predicted, I was released from the hospital the same day as my surgery and remarkably pain-free. I took one Tramadol (a step down from stronger medications containing codeine) when I got home — only because it was suggested I take one pill. As I recovered, I only took Advil and Tylenol. The opioid epidemic is a major public health issue in the United States and nerve blocks could be a solution. According to a study published in the Journal of Clinical Medicine in 2021, 1 in 20 surgical patients will continue to use opioids beyond 90 days. “There is no association with magnitude of surgery, major versus minor, and the strongest predictor of continued use is surgical exposure,” the study states. © 1996-2022 The Washington Post

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: 28316 - Posted: 05.07.2022

By Jim Robbins TUCSON, Ariz. — In a small room in a building at the Arizona-Sonora Desert Museum, the invertebrate keeper, Emma Califf, lifts up a rock in a plastic box. “This is one of our desert hairies,” she said, exposing a three-inch-long scorpion, its tail arced over its back. “The largest scorpion in North America.” This captive hairy, along with a swarm of inch-long bark scorpions in another box, and two dozen rattlesnakes of varying species and sub- species across the hall, are kept here for the coin of the realm: their venom. Efforts to tease apart the vast swarm of proteins in venom — a field called venomics — have burgeoned in recent years, and the growing catalog of compounds has led to a number of drug discoveries. As the components of these natural toxins continue to be assayed by evolving technologies, the number of promising molecules is also growing. “A century ago we thought venom had three or four components, and now we know just one type of venom can have thousands,” said Leslie V. Boyer, a professor emeritus of pathology at the University of Arizona. “Things are accelerating because a small number of very good laboratories have been pumping out information that everyone else can now use to make discoveries.” She added, “There’s a pharmacopoeia out there waiting to be explored.” It is a striking case of modern-day scientific alchemy: The most highly evolved of natural poisons on the planet are creating a number of effective medicines with the potential for many more. One of the most promising venom-derived drugs to date comes from the deadly Fraser Island funnel web spider of Australia, which halts cell death after a heart attack. Blood flow to the heart is reduced after a heart attack, which makes the cell environment more acidic and leads to cell death. The drug, a protein called Hi1A, is scheduled for clinical trials next year. In the lab, it was tested on the cells of beating human hearts. It was found to block their ability to sense acid, “so the death message is blocked, cell death is reduced, and we see improved heart cell survival,” said Nathan Palpant, a researcher at the University of Queensland in Australia who helped make the discovery. © 2022 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: 28315 - Posted: 05.04.2022

Ellen Phiddian Tricyclic antidepressants have long been known to have more than one purpose: among other things, they can alleviate pain – particularly nerve pain. Recent research has finally established why these tricyclic antidepressants (TCAs) can help with nerve pain. The discovery could lead to the rapid development of pain relief medications that don’t include the side effects of TCAs. Nerve pain comes from a variety of sources – including cancer, diabetes, trauma, multiple sclerosis, and infections. These treatments could address a range of different types of nerve pain. It turns out the drugs inhibit a key protein in our nerves, called an N-type calcium channel. These N-type calcium channels are shaped like tiny gates, allowing positively charged calcium ions, or Ca2+, through them. This helps with the transmission of pain signals in the body. Researchers have long been keen to find things that “close” the gate of these calcium channels because that’s likely to have analgesic effects. Adjunct Professor Peter Duggan, a researcher with the CSIRO and senior collaborator on the project, says that he and his colleagues initially stumbled across TCAs from a very different direction: they were investigating the toxins of venomous marine cone snails. “A few of the components in that toxin are actually painkillers and they block these calcium ion channels very, very effectively,” says Duggan. The cone snail toxin has the potential to be very dangerous to people, as well as needing to be administered in an impractical way, so the researchers started looking at similar compounds that might have some of the same properties.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28312 - Posted: 05.04.2022

By Helen Ouyang After an hour-and-a-half bus ride last November, Julia Monterroso arrived at a white Art Deco building in West Hollywood, just opposite a Chanel store and the Ivy, a restaurant famous for its celebrity sightings. Monterroso was there to see Brennan Spiegel, a gastroenterologist and researcher at Cedars-Sinai who runs one of the largest academic medical initiatives studying virtual reality as a health therapy. He started the program in 2015 after the hospital received a million-dollar donation from an investment banker on its board. Spiegel saw Monterroso in his clinic the week before and thought he might be able to help alleviate her symptoms. Monterroso is 55 and petite, with youthful bangs and hair clipped back by tiny jeweled barrettes. Eighteen months earlier, pain seized her lower abdomen and never went away. After undergoing back surgery in September to treat a herniated disc — and after the constant ache in her abdomen worsened — she had to stop working as a housecleaner. Eventually, following a series of tests that failed to reveal any clear cause, she landed in Spiegel’s office. She rated her pain an 8 on a 10-point scale, with 10 being the most severe. Chronic pain is generally defined as pain that has lasted three months or longer. It is one of the leading causes of long-term disability in the world. By some measures, 50 million Americans live with chronic pain, in part because the power of medicine to relieve pain remains woefully inadequate. As Daniel Clauw, who runs the Chronic Pain and Fatigue Research Center at the University of Michigan, put it in a 2019 lecture, there isn’t “any drug in any chronic-pain state that works in better than one out of three people.” He went on to say that nonpharmacological therapy should instead be “front and center in managing chronic pain — rather than opioids, or for that matter, any of our drugs.” Virtual reality is emerging as an unlikely tool for solving this intractable problem. The V.R. segment in health care alone, which according to some estimates is already valued at billions of dollars, is expected to grow by multiples of that in the next few years, with researchers seeing potential for it to help with everything from anxiety and depression to rehabilitation after strokes to surgeons strategizing where they will cut and stitch. In November, the Food and Drug Administration gave authorization for the first V.R. product to be marketed for the treatment of chronic pain. © 2022 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 7: Vision: From Eye to Brain
Link ID: 28304 - Posted: 04.27.2022

By Brittany Shammas and Timothy Bella William Husel, an Ohio doctor who was accused of killing 14 patients with what prosecutors described as “wildly excessive” doses of fentanyl between 2015 and 2018, was acquitted on all counts of murder Wednesday, concluding one of the most significant murder cases of its kind against a health-care professional. Husel, a onetime physician of the year trained at the Cleveland Clinic, faced one count of murder for each of the 14 critically ill patients he was accused of killing. The jury deliberated for seven days before finding him not guilty on all 14 counts in what was one of the largest murder trials in Ohio history. He had been charged with causing or hastening their deaths amid a period of lax oversight of fentanyl at Mount Carmel West, a Catholic hospital in Columbus. Husel would have faced life in prison with just one guilty verdict. While the synthetic opioid is significantly more powerful than morphine and has wreaked havoc on American streets, it can provide pain relief in medical settings that is crucial to end-of-life care. The alleged victims in the Ohio case suffered critical medical conditions including overdoses, cancer, strokes and internal bleeding. Prosecutors acknowledged that all were being kept alive on ventilators and that many of them were dying. “In truth, William Husel was an innocent man, and thank goodness the justice system prevailed,” Jose Baez, one of Husel’s defense attorneys, told reporters. The 46-year-old’s acquittal came after a two-month trial that triggered a debate on end-of-life medical care. Husel and Baez argued in the trial that the doctor offered comfort care for dying patients and was not trying to kill them. They pointed out that the doctor’s actions did not occur in secret — nurses were the ones to administer the doses — and alleged that hospital officials made Husel the villain after realizing the systemic failures at play. The fallout over the allegations at Mount Carmel West had repercussions: the firing of 23 employees; the resignation of the hospital’s chief executive, chief clinical officer and chief pharmacy officer; and Medicare and Medicaid funding for the institution was put in jeopardy. © 1996-2022 The Washington Post

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: 28297 - Posted: 04.23.2022

ByKelly Servick An experimental pain drug that may offer an alternative to opioids has shown promise in two small clinical trials for acute pain, its developer announced today. Vertex Pharmaceuticals’s compound, called VX-548, outperformed a placebo in phase 2 trials for two types of postsurgical pain, the company said in a press release. The results pave the way for larger trials that could lead to regulatory approval. “This is a major advance in the effort to supersede opioids,” says John Wood, a neurobiologist at University College London who has studied the cellular channel that VX-548 targets. “These results are terrific, and the side effect profile is very good.” Opioids are powerful pain relievers, but they can cause side effects including slowed breathing, and they come with the potential for addiction. An epidemic of overdose deaths has prompted a hunt for safer alternatives. The new trials grew out of research into sodium channels on the surface of pain-sensing neurons, which let them fire electrical signals. One such channel, called Nav1.8, is crucial to relaying pain signals to the spinal cord from nerves throughout the body. People with genetic mutations that make Nav1.8 hyperactive can suffer pain even in the absence of injury. But relieving pain by blocking either Nav1.8 or another channel, Nav1.7, has proved difficult. One issue is their structure closely resembles those of other sodium channels, which regulate vital functions in the heart, muscles, and brain. To be safe, a compound needs to target the channel of interest and not accidentally target these other, critical channels. Vertex has spent years developing highly specific Nav1.8-blocking drugs, but it has abandoned previous candidates before they reached pivotal phase 3 trials. One drug, known as VX-150, succeeded in three phase 2 clinical studies but never advanced to larger ones, in part because its high dose might be impractical for clinical use. “We wanted to have higher potency,” explains Vertex Chief Scientific Officer David Altshuler. © 2022 American Association for the Advancement of Science.

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: 28265 - Posted: 04.02.2022

By Lisa Sanders, M.D. The 51-year-old man sat at his desk preparing for his next online meeting when he suddenly became aware of a familiar stiffness and exhaustion. Had he slept badly? Or was this the beginning of one of his strange episodes? As the symptoms worsened, he had his answer. He knew that when he started to feel this way, the only recourse was to get into bed before he got any weaker. As he made his way slowly down the hall, his legs felt heavy, as if he were wearing ankle weights. Just lifting them was real work. He passed his wife’s home office without a word. She knew just from looking at him that he would probably have to spend the rest of the day in bed. For much of their 30-year marriage, he had these strange spells; he would suddenly feel exhausted and weak and have to lie down. He couldn’t work. He was a software engineer, and any mental exertion was too much for him. Once the fatigue fully set in — maybe after the first hour or so — he couldn’t walk, couldn’t stand, couldn’t even sit up. It was as if his body was totally out of gas, worse than how it felt when he ran a marathon. He would lie in a dark room, too weak to even hold up a book and too tired to think. But by the next morning, he would usually be fine, brimming with energy and enthusiasm, like normal. It was so strange. After more than 20 years, they both had come to expect these episodes. For most of that time, the spells were infrequent, maybe once a month. But recently they became more frequent. The monthly episodes became weekly, then a couple of times a week. They often came, as they did that morning, out of nowhere. Just before leaving his office, he sent an email to the woman he was to meet online. Sorry, he wrote, I’m not feeling well. Could we reschedule? Seeing a Psychiatrist Over the years the man saw many doctors. They had their theories, but so far none panned out. A few were convinced that he had periodic paralysis, a disorder sometimes linked to thyroid disease, where patients become temporarily paralyzed by too much or too little potassium in the bloodstream. But his potassium was always normal, even during these episodes. © 2022 The New York Times Company

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: 28263 - Posted: 04.02.2022

Chloe Tenn On October 4, physiologist David Julius and neurobiologist Arden Patapoutian were awarded the Nobel Prize in Physiology or Medicine for their work on temperature, pain, and touch perception. Julius researched the burning sensation people experience from chilies, and identified an ion channel, TRPV1 that is activated by heat. Julius and Patapoutian then separately reported on the TRPM8 ion channel that senses menthol’s cold in 2002. Patapoutian’s group went on to discover the PIEZO1 and PIEZO2 ion channels that are involved in sensing mechanical pressure. The Nobel Committee wrote that the pair’s work inspired further research into understanding how the nervous system senses temperature and mechanical stimuli and that the laureates “identified critical missing links in our understanding of the complex interplay between our senses and the environment.” This year saw innovations in augmenting the brain’s capabilities by plugging it in to advanced computing technology. For example, a biology teacher who lost her vision 16 years ago was able to distinguish shapes and letters with the help of special glasses that interfaced with electrodes implanted in her brain. Along a similar vein, a computer connected to a brain-implant system discerned brain signals for handwriting in a paralyzed man, enabling him to type up to 90 characters per minute with an accuracy above 90 percent. Such studies are a step forward for technologies that marry cutting-edge neuroscience and computational innovation in an attempt to improve people’s lives. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Lateralization
Link ID: 28134 - Posted: 12.31.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

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: 28120 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

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: 28117 - Posted: 12.18.2021

By Lisa Sanders, M.D. The 66-year-old man had just started his third lap at the community swimming pool outside Poughkeepsie, N.Y., when it struck. As he was turning his head to take a breath, an octopus of pain wrapped around the right side of his skull, starting at the joint where the jaw connects and slamming across his face and head with tentacles of squeezing agony. For a moment he was paralyzed — first with pain, then with fear. He couldn’t breathe; he could barely move. He struggled to the side of the pool and hung on, his breath ragged through involuntarily clenched teeth. His wife hurried over. He was a good swimmer; what was wrong? She saw his lips move and leaned closer. His jaw was clenched. “I can’t speak,” he mumbled. She helped him out of the pool. “We’re going to go to urgent care,” she said as she handed him a towel. These strange pains had been tormenting the man for nearly three weeks. It started as a headache that woke him from a dead sleep, a squeezing pressure deep inside his brain. He got up and took some acetaminophen. When he awoke the next morning, the headache was gone, but the regions around his head and face where the pressure had been strongest felt strangely tender. He couldn’t even brush his hair on the right side of his head. Bizarre as this was, he most likely would have soon forgotten about it except that it happened again the next night — and just about every night since. The pain in his jaw started a couple of days later. Opening and closing his mouth, and especially chewing, made his jaw throb. Eating anything more solid than mashed potatoes triggered excruciating pain. He went to his dentist, who poked and prodded. The only tenderness was in the joint where the jaw attached to the skull. It’s most likely TMJ, the dentist concluded — temporomandibular joint pain. That joint and the many attached muscles make speech and facial expressions possible. Lots of people have pain there, the dentist added. Bad habits like jaw-clenching and tooth-grinding aggravate the joint. The treatment is behavior modification to unlearn these habits, and sometimes a bite block, a custom-made piece of acrylic worn at night to protect teeth from injury. © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28113 - Posted: 12.15.2021

By David Dobbs Chronic pain is both one of the world’s most costly medical problems, affecting one in every five people, and one of the most mysterious. In the past two decades, however, discoveries about the crucial role played by glia — a set of nervous system cells once thought to be mere supports for neurons — have rewritten chronic pain science. These findings have given patients and doctors a hard-science explanation that chronic pain previously lacked. By doing so, this emerging science of chronic pain is beginning to influence care — not by creating new treatments, but by legitimizing chronic pain so that doctors take it more seriously. Although glia are scattered throughout the nervous system and take up almost half its space, they long received far less scientific attention than neurons, which do the majority of signaling in the brain and body. Some types of glia resemble neurons, with roughly starfish-like bodies, while others look like structures built with Erector sets, their long, straight structural parts joined at nodes. When first discovered in the mid-1800s, glia — from the Greek word for glue — were thought to be just connective tissue holding neurons together. Later they were rebranded as the nervous system’s janitorial staff, as they were found to feed neurons, clean up their waste and take out their dead. In the 1990s they were likened to secretarial staff when it was discovered they also help neurons communicate. Research over the past 20 years, however, has shown that glia don’t just support and respond to neuronal activity like pain signals — they often direct it, with enormous consequences for chronic pain. If you’re hearing this for the first time and you’re one of the billion-plus people on Earth who suffer from chronic pain (meaning pain lasting beyond three to six months that has no apparent cause or has become independent of the injury or illness that caused it), you might be tempted to say that your glia are botching their pain-management job. © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28075 - Posted: 11.13.2021

By James Gallagher An innovative type of medicine - called gene silencing - is set to be used on the NHS for people who live in crippling pain. The drug treats acute intermittent porphyria, which runs in families and can leave people unable to work or have a normal life. Clinical trials have shown severe symptoms were cut by 74% with the drug. While porphyria is rare, experts say the field of gene silencing has the potential to revolutionise medicine. Sisters Liz Gill and Sue Burrell have both had their lives turned around by gene silencing. Before treatment, Liz, from County Durham, remembers the trauma of living in "total pain" and, at its worst, she spent two years paralysed in hospital. Younger sister Sue says she "lost it all overnight" when she was suddenly in and out of hospital, made redundant and did know whether her partner would stick with her (he did). "It was scary," she tells me. Both became used to taking potent opioid painkillers on a daily basis. But even morphine could not block the pain during a severe attack that needed hospital treatment. Gene silencing gets to the root-cause of the sisters' disease rather than just managing their symptoms. Their porphyria leads to a build-up of toxic proteins in the body, that cause the physical pain. Gene silencing "mutes" a set of genetic instructions to block that protein production. Both had been taking the therapy as part of a clinical trial and are still getting monthly injections. © 2021 BBC.

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: 28046 - Posted: 10.23.2021

Brenda Patoine Science likes to package its successes in neat stories that show a clear progression from this to that. The “bench-to-bedside” story—when biological insights yield targeted treatments—is a long-time favorite. Reality, however, doesn’t always cooperate, and history is littered with basic-science discoveries that seemed important but failed to yield viable treatments. When they do succeed, it’s cause for celebration—and awards. Migraine research is an example. Although it is the second most disabling condition in the world, affecting one billion people, migraine had long been relegated to the backwaters of scientific research. Only recently has research bloomed—scientific papers sharply increased from the 1990s onward, with discoveries in basic science driving a new class of drugs that some in the field are calling game changers. This year, the recognition of four migraine researchers with a major neuroscience award has pushed the field into the limelight of science. The 2021 Brain Prize recognizes science that embodies the so-called bench-to-bedside research described above. That’s a jargony term scientists seem to love that denotes the rare and wonderful occurrence when laboratory research aimed at illuminating fundamental mechanisms (the “bench”) yields insights that lead to drugs that ultimately help millions of sick people (the “bedside”). In the case of migraine research, the leading character is a neuropeptide called calcitonin gene-related peptide (CGRP). © 2021 The Dana Foundation.

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: 28040 - Posted: 10.16.2021