Chapter 5. The Sensorimotor System

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By Christina Jewett Just four months ago, Noland Arbaugh had a circle of bone removed from his skull and hair-thin sensor tentacles slipped into his brain. A computer about the size of a small stack of quarters was placed on top and the hole was sealed. Paralyzed below the neck, Mr. Arbaugh is the first patient to take part in the clinical trial of humans testing Elon Musk’s Neuralink device, and his early progress was greeted with excitement. Working with engineers, Mr. Arbaugh, 30, trained computer programs to translate the firing of neurons in his brain into the act of moving a cursor up, down and around. His command of the cursor was soon so agile that he could challenge his stepfather at Mario Kart and play an empire-building video game late into the night. But as weeks passed, about 85 percent of the device’s tendrils slipped out of his brain. Neuralink’s staff had to retool the system to allow him to regain command of the cursor. Though he needed to learn a new method to click on something, he can still skate the cursor across the screen. Neuralink advised him against a surgery to replace the threads, he said, adding that the situation had stabilized. The setback became public earlier this month. And although the diminished activity was initially difficult and disappointing, Mr. Arbaugh said it had been worth it for Neuralink to move forward in a tech-medical field aimed at helping people regain their speech, sight or movement. “I just want to bring everyone along this journey with me,” he said. “I want to show everyone how amazing this is. And it’s just been so rewarding. So I’m really excited to keep going.” From a small desert town in Arizona, Mr. Arbaugh has emerged as an enthusiastic spokesman for Neuralink, one of at least five companies leveraging decades of academic research to engineer a device that can help restore function in people with disabilities or degenerative diseases. © 2024 The New York Times Company

Keyword: Robotics
Link ID: 29320 - Posted: 05.23.2024

By Meghan Willcoxon In the summer of 1991, the neuroscientist Vittorio Gallese was studying how movement is represented in the brain when he noticed something odd. He and his research adviser, Giacomo Rizzolatti, at the University of Parma were tracking which neurons became active when monkeys interacted with certain objects. As the scientists had observed before, the same neurons fired when the monkeys either noticed the objects or picked them up. But then the neurons did something the researchers didn’t expect. Before the formal start of the experiment, Gallese grasped the objects to show them to a monkey. At that moment, the activity spiked in the same neurons that had fired when the monkey grasped the objects. It was the first time anyone had observed neurons encode information for both an action and another individual performing that action. Those neurons reminded the researchers of a mirror: Actions the monkeys observed were reflected in their brains through these peculiar motor cells. In 1992, Gallese and Rizzolatti first described the cells in the journal Experimental Brain Research and then in 1996 named them “mirror neurons” in Brain. The researchers knew they had found something interesting, but nothing could have prepared them for how the rest of the world would respond. Within 10 years of the discovery, the idea of a mirror neuron had become the rare neuroscience concept to capture the public imagination. From 2002 to 2009, scientists across disciplines joined science popularizers in sensationalizing these cells, attributing more properties to them to explain such complex human behaviors as empathy, altruism, learning, imitation, autism, and speech. Then, nearly as quickly as mirror neurons caught on, scientific doubts about their explanatory power crept in. Within a few years, these celebrity cells were filed away in the drawer of over-promised, under-delivered discoveries. © 2024 NautilusNext Inc.,

Keyword: Attention; Vision
Link ID: 29316 - Posted: 05.21.2024

Ian Sample Science editor A device that stimulates the spinal nerves with electrical pulses appears to boost how well people recover from major spinal cord injuries, doctors say. An international trial found that patients who had lost some or all use of their hands and arms after a spinal cord injury regained strength, control and sensation when the stimulation was applied during standard rehabilitation exercises. The improvements were small but were described by doctors and patients as life-changing because of the impact they had on the patients’ daily routines and quality of life. “It actually makes it easier for people to move, including people who have complete loss of movement in their hands and arms,” said Prof Chet Moritz, in the department of rehabilitation medicine at the University of Washington in Seattle. “The benefits accumulate gradually over time as we pair this spinal stimulation with intensive therapy of the hands and arms, such that there are benefits even when the stimulator is turned off.” Rather than being implanted, the Arc-Ex device is worn externally and uses electrodes that are placed on the skin near the section of the spinal cord responsible for controlling a particular movement or function. The researchers believe that electrical stimulation helps nerves that remain intact after the injury to send signals and ultimately partially restore some communication between the brain and paralysed body part. More than half of patients who suffer spinal cord injuries still have some intact nerves that cross the injury site. © 2024 Guardian News & Media Limited

Keyword: Robotics; Movement Disorders
Link ID: 29315 - Posted: 05.21.2024

By Kermit Pattison Since the Stone Age, hunters have brought down big game with spears, atlatls, and bows and arrows. Now, a new study reveals traditional societies around the globe also relied on another deadly but often-overlooked weapon: our legs. According to a report published today in Nature Human Behaviour, running down big game such as antelope, moose, and even kangaroos was far more widespread than previously recognized. Researchers documented nearly 400 cases of endurance pursuits—a technique in which prey are chased to exhaustion—by Indigenous peoples around the globe between the 16th and 21st centuries. And in some cases, they suggest, it can be more efficient than stealthy stalking. The findings bolster the idea that humans evolved to be hunting harriers, says Daniel Lieberman, an evolutionary biologist at Harvard University. “Nobody else has come up with any other explanation for why humans evolved to run long distances,” says Lieberman, who adds that he’s impressed with the paper’s “depth of scholarship.” For decades, some anthropologists have argued that endurance running was among the first hunting techniques employed by early hominins in Africa. Advocates suggest subsequent millennia spent chasing down prey shaped many unique human features, including our springy arched feet, slow-twitch muscle fibers optimized for efficiency, heat-shedding bare skin, and prodigious ability to sweat. The “born to run” idea has become something of an origin story among many endurance athletes. But a pack of skeptics has dogged the theory. Critics cited the higher energetic costs of running over walking and noted that accounts of persistence hunting among modern foragers are rare. Yet hints of such pursuits kept popping up as Eugène Morin, an archaeologist at Trent University and co-author of the new paper, scoured the literature for a book he was writing on hunting among traditional societies. As he pored over early accounts by missionaries, travelers, and explorers, he repeatedly found descriptions of long-distance running and tracking. © 2024 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 29309 - Posted: 05.16.2024

By J. David Creswell Let’s start thinking differently about exercise. Decades of exercise science research show that when people or animals are given a new exercise routine, they get healthier. But when thinking about the benefits of exercise, most people hold a strong body bias; they focus on how regular exercise builds more lean body mass, helps increase their strength and balance, or improves heart health. Exercise matters even more for our brains, it turns out, in ways that are often overlooked. Here’s how we know. Animal exercise studies typically run rats for weeks on running wheels. The animals gleefully run every night, sprinting several miles over the course of an evening. There are wonderful health benefits in these studies of voluntary running—improved muscle tone and cardiovascular health, and many brain benefits too. But in some studies, there’s an additional experimental condition where some rats exercise with one crucial difference: it’s no longer voluntary exercise. Instead of a freestanding running wheel, rats run on a mechanized wheel that spins, forcing the animals to cover the same distance as the voluntary runners. What happens? When the rats are forced to exercise on a daily basis for several weeks, their bodies become more physically fit, but their brains suffer. Animals regularly forced to exercise have the equivalent of an anxiety disorder, behaving on new tasks in highly anxious and avoidant ways. These animals are more anxious not only compared to the voluntary runners, but also to animals that are not given an opportunity to exercise at all. Yes, forced exercise might be worse than no exercise at all. This work suggests something important about the health benefits of exercise: it is not just about making our muscles work, but what exercise does to our brains. When exercise gives us a sense of control, mastery and joy, our brains become less anxious. If we take that away, by forcing exercise, we can shift it from helpful to harmful. © 2024 SCIENTIFIC AMERICAN,

Keyword: Stress; Depression
Link ID: 29284 - Posted: 05.02.2024

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.

Keyword: Pain & Touch; Emotions
Link ID: 29262 - Posted: 04.20.2024

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

Keyword: Pain & Touch; Emotions
Link ID: 29252 - Posted: 04.11.2024

Matthew Farrer Parkinson’s disease is a neurodegenerative movement disorder that progresses relentlessly. It gradually impairs a person’s ability to function until they ultimately become immobile and often develop dementia. In the U.S. alone, over a million people are afflicted with Parkinson’s, and new cases and overall numbers are steadily increasing. There is currently no treatment to slow or halt Parkinson’s disease. Available drugs don’t slow disease progression and can treat only certain symptoms. Medications that work early in the disease, however, such as Levodopa, generally become ineffective over the years, necessitating increased doses that can lead to disabling side effects. Without understanding the fundamental molecular cause of Parkinson’s, it’s improbable that researchers will be able to develop a medication to stop the disease from steadily worsening in patients. Many factors may contribute to the development of Parkinson’s, both environmental and genetic. Until recently, underlying genetic causes of the disease were unknown. Most cases of Parkinson’s aren’t inherited but sporadic, and early studies suggested a genetic basis was improbable. Nevertheless, everything in biology has a genetic foundation. As a geneticist and molecular neuroscientist, I have devoted my career to predicting and preventing Parkinson’s disease. In our newly published research, my team and I discovered a new genetic variant linked to Parkinson’s that sheds light on the evolutionary origin of multiple forms of familial parkinsonism, opening doors to better understand and treat the disease. In the mid-1990s, researchers started looking into whether genetic differences between people with or without Parkinson’s might identify specific genes or genetic variants that cause the disease. In general, I and other geneticists use two approaches to map the genetic blueprint of Parkinson’s: linkage analysis and association studies. © 2010–2024, The Conversation US, Inc.

Keyword: Parkinsons; Genes & Behavior
Link ID: 29249 - Posted: 04.11.2024

By David Adam A diabetes drug related to the latest generation of obesity drugs can slow the development of the symptoms of Parkinson’s disease, a clinical trial suggests1. Participants who took the drug, called lixisenatide, for 12 months showed no worsening of their symptoms — a gain in a condition marked by progressive loss of motor control. Further work is needed to control side effects and determine the best dose, but researchers say that the trial marks another promising step in the decades-long effort to tackle the common and debilitating disorder. “This is the first large-scale, multicentre clinical trial to provide the signs of efficacy that have been sought for so many years,” says Olivier Rascol, a Parkinson’s researcher at Toulouse University Hospital in France, who led the study. The diabetes connection Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist, making it part of a large family of similar compounds used to treat diabetes and, more recently, obesity. (The weight-loss drug semaglutide, sold under the brand name Wegovy, is a GLP-1 compound.) Many studies have shown a link between diabetes and Parkinson’s2. People with diabetes are around 40% more likely to develop Parkinson’s. And people who have both Parkinson’s and diabetes often see more rapid progression of symptoms than do those who have only Parkinson’s. Animal studies3 have suggested that some GLP-1 drugs, which influence levels of insulin and glucose, can slow the symptoms of Parkinson’s. Smaller trials, published in 20134 and 20175, suggested that the GLP-1 molecule exenatide, another diabetes drug, could do the same in people.

Keyword: Parkinsons
Link ID: 29240 - Posted: 04.04.2024

By Emily Makowski & I spend my days surrounded by thousands of written words, and sometimes I feel as though there’s no escape. That may not seem particularly unusual. Plenty of people have similar feelings. But no, I’m not just talking about my job as a copy editor here at Scientific American, where I edit and fact-check an endless stream of science writing. This constant flow of text is all in my head. My brain automatically translates spoken words into written ones in my mind’s eye. I “see” subtitles that I can’t turn off whenever I talk or hear someone else talking. This same speech-to-text conversion even happens for the inner dialogue of my thoughts. This mental closed-captioning has accompanied me since late toddlerhood, almost as far back as my earliest childhood memories. And for a long time, I thought that everyone could “read” spoken words in their head the way I do. What I experience goes by the name of ticker-tape synesthesia. It is not a medical condition—it’s just a distinctive way of perceiving the surrounding world that relatively few people share. Not much is known about the neurophysiology or psychology of this phenomenon, sometimes called “ticker taping,” even though a reference to it first appeared in the scientific literature in the late 19th century. Ticker taping is considered a form of synesthesia, an experience in which the brain reroutes one kind of incoming sensory information so that it is processed as another. For example, sounds might be perceived as touch, allowing the affected person to “feel” them as tactile sensations. As synesthesia goes, ticker taping is relatively uncommon. “There are varieties of synesthesia which really have just been completely under the radar..., and ticker tape is really one of those,” says Mark Price, a cognitive psychologist at the University of Bergen in Norway. The name “ticker-tape synesthesia” itself evokes the concept’s late 19th-century origins. At that time stock prices transmitted by telegraph were printed on long paper strips, which would be torn into tiny bits and thrown from building windows during parades. © 2024 SCIENTIFIC AMERICAN,

Keyword: Attention; Language
Link ID: 29238 - Posted: 04.04.2024

By Javier C. Hernández The pianist Alice Sara Ott, barefoot and wearing a silver bracelet, was smiling and singing to herself the other day as she practiced a jazzy passage of Ravel at Steinway Hall in Midtown Manhattan. A Nintendo Switch, which she uses to warm up her hands, was by her side (another favored tool is a Rubik’s Cube). A shot of espresso sat untouched on the floor. “I feel I have finally found my voice,” Ott said during a break. “I feel I can finally be myself.” Ott, 35, who makes her New York Philharmonic debut this week, has built a global career, recording more than a dozen albums and appearing with top ensembles. She has become a force for change in classical music, embracing new approaches (playing Chopin on beat-up pianos in Iceland) and railing against stuffy concert culture (she performs without shoes, finding it more comfortable). And Ott, who lives in Munich and has roots in Germany and Japan, has done so while grappling with illness. In 2019, when she was 30, she was diagnosed with multiple sclerosis. She says she has not shown any symptoms since starting treatment, but the disorder has made her reflect on the music industry’s grueling work culture. “I learned to accept that there is a limit and to not go beyond that,” she said. “Everybody knows how to ignore their body and just go on. But there’s always a payback.” Ott has used her platform to help dispel myths about multiple sclerosis, a disorder of the central nervous system that can cause a wide range of symptoms, including muscle spasms, numbness and vision problems. She has taken to social media to detail her struggles and to challenge those who have suggested that the illness has affected her playing. She said she felt she had no choice but to be transparent, saying it was important to show that people with multiple sclerosis could lead full lives. “I don’t consider it as a weakness,” she said. “It’s a fact. I live with it. And I don’t want to make a big drama out of it.” © 2024 The New York Times Company

Keyword: Multiple Sclerosis
Link ID: 29237 - Posted: 04.04.2024

By Tina Hesman Saey Atoosa Samani started learning about pigeon genetics at a young age. She grew up surrounded by pet pigeons in Isfahan, a city in central Iran famed for its pigeon towers. Her favorite was an all-white bird. But 6- or 7-year-old Samani noticed that this particular pigeon never fathered all-white offspring. She learned that white coloring is a recessive genetic trait — one that shows up only when an individual inherits two broken copies of a gene (SN: 2/7/22). In this case, the pigeon had two broken copies of a gene that normally makes pigment to color feathers, so his feathers were white. But his offspring inherited a normal, pigment-producing version of the gene from their mothers and had colored feathers. That early lesson in pigeon heredity stuck with Samani and fueled her desire to learn more about genetics. When she moved to the United States to study at the University of Utah in Salt Lake City, it seemed only natural to join Michael Shapiro’s lab to investigate why some pigeons (Columba livia) do backward somersaults (SN: 1/31/13). These roller pigeons come in two varieties: Flying rollers such as Birmingham rollers, which fly but do long tumbling runs toward the ground before resuming flight, and parlor rollers, which can’t fly but instead backflip along the ground. Many Persian poems say the pigeons perform the acrobatics because the birds are happy, but Samani says the truth is darker. “This is definitely a movement disorder, and it does not have any good aspects to it,” she says. The disorder is progressive, appearing soon after hatching and gradually getting worse until the birds can’t fly. © Society for Science & the Public 2000–2024.

Keyword: Movement Disorders; Genes & Behavior
Link ID: 29235 - Posted: 04.02.2024

By James Gaines A lethal, incurable malady similar to mad cow disease is sweeping across deer species in North America and starting to spread around the world. First identified in a single herd of captive mule deer in Colorado in 1967, chronic wasting disease — CWD — has now been found in captive and wild mule deer, white-tailed deer, elk, moose and reindeer. It’s been found in 32 states and has crossed international boundaries into Canada, South Korea and Norway, among other countries. The disease — caused by a rogue protein known as a prion — has not yet been shown to infect humans, though fears remain. But even if that never happens, CWD could kill off large numbers of deer and possibly wipe out individual populations. Wildlife management agencies may, in turn, introduce stricter hunting rules, and the fear of contaminated meat could scare away potential hunters, affecting the United States’ roughly $23 billion deer hunting industry. Since CWD’s emergence, scientists have been working to understand the disease and how it might be brought under control. Over the years, three potential mitigation strategies have emerged, but each has significant challenges. Nicholas Haley, a veterinary microbiologist at Midwestern University in Arizona, coauthored an overview of chronic wasting disease in the 2015 Annual Review of Animal Biosciences and has been working on the problem ever since. Knowable Magazine spoke with Haley about the options and whether we can ever contain the disease. What’s a prion disease? CWD isn’t caused by a bacterium or virus, but by a naturally occurring protein in our cells twisting out of shape.

Keyword: Prions
Link ID: 29232 - Posted: 04.02.2024

By Marta Zaraska The renowned Polish piano duo Marek and Wacek didn’t use sheet music when playing live concerts. And yet onstage the pair appeared perfectly in sync. On adjacent pianos, they playfully picked up various musical themes, blended classical music with jazz and improvised in real time. “We went with the flow,” said Marek Tomaszewski, who performed with Wacek Kisielewski until Wacek’s death in 1986. “It was pure fun.” The pianists seemed to read each other’s minds by exchanging looks. It was, Marek said, as if they were on the same wavelength. A growing body of research suggests that might have been literally true. Dozens of recent experiments studying the brain activity of people performing and working together — duetting pianists, card players, teachers and students, jigsaw puzzlers and others — show that their brain waves can align in a phenomenon known as interpersonal neural synchronization, also known as interbrain synchrony. “There’s now a lot of research that shows that people interacting together display coordinated neural activities,” said Giacomo Novembre, a cognitive neuroscientist at the Italian Institute of Technology in Rome, who published a key paper on interpersonal neural synchronization last summer. The studies have come out at an increasing clip over the past few years — one as recently as last week — as new tools and improved techniques have honed the science and theory. They’re finding that synchrony between brains has benefits. It’s linked to better problem-solving, learning and cooperation, and even with behaviors that help others at a personal cost. What’s more, recent studies in which brains were stimulated with an electric current hint that synchrony itself might cause the improved performance observed by scientists. © 2024 the Simons Foundation.

Keyword: Attention
Link ID: 29229 - Posted: 03.30.2024

By Saugat Bolakhe For desert ants, Earth’s magnetic field isn’t just a compass: It may also sculpt their brains. Stepping outside their nest for the first time, young ants need to learn how to forage. The ants train partly by walking a loop near their nests for the first three days. During this stroll, they repeatedly pause and then pirouette to gaze back at the nest entrance, learning how to find their way back home. But when the magnetic field around the nest entrance was disturbed, ant apprentices couldn’t figure out where to look, often gazing in random directions, researchers report in the Feb. 20 Proceedings of the National Academy of Sciences. What’s more, the altered magnetic field seemed to affect connections between neurons in the learning and memory centers in the young ants’ brains. The finding “may make it easier to better understand how magnetic fields are sensed [in animals]” as scientists now know one way that magnetic fields can influence brain development, says Robin Grob, a biologist at the Norwegian University of Science and Technology in Trondheim. For years, scientists have known that some species of birds, fishes, turtles, moths and butterflies rely on Earth’s magnetic field to navigate (SN: 4/3/18). In 2018, Grob and other scientists added desert ants to that list. Young ants first appeared to use the magnetic field as a reference while learning how to use landmarks and the sun as guides to orient themselves in the right direction to gaze back toward the nest with its small, hard-to-see entrance. However, knowing where in the brain magnetic cues are processed has proved challenging. © Society for Science & the Public 2000–2024.

Keyword: Animal Migration; Development of the Brain
Link ID: 29227 - Posted: 03.30.2024

By Dennis Normile By the time a person shows symptoms of Parkinson’s disease, neurons in a part of their brain key to movement have already quietly died. To learn how this process unfolds, identify warning signs, and test treatments, researchers have long wanted an animal model of the disease’s early stages. Now, they may have one: a cohort of transgenic marmosets, described at a conference on nonhuman primate models in Hong Kong last month. The animals, which neuroscientist Hideyuki Okano of Keio University and colleagues created using a mutated protein that seems to drive Parkinson’s in some people, closely mimic the disease’s onset and progression. And they have enabled Okano’s team to identify what could be an early, predictive sign of disease in brain imaging. The model could be “transformative” for Parkinson’s studies, says neurobiologist Peter Strick of the University of Pittsburgh, who attended the meeting, organized by the Hong Kong University of Science and Technology, Stanford University, and the University of California San Francisco. “We desperately need nonhuman primate models that recapitulate the natural onset and progression” of conditions like Parkinson’s, he says. Parkinson’s, which afflicts an estimated 8.5 million people, is thought to be triggered by a combination of genetic and environmental factors, such as exposure to toxic chemicals. It sets in as neurons that produce the chemical messenger dopamine in the substantia nigra, an area of the brain that controls movement, die off. Early symptoms include tremors, muscle stiffness, and hesitant motions. The disease can later affect cognition and lead to dementia. Researchers think one cause of neuronal death may be abnormal versions of a protein called alpha-synuclein that misfold and form toxic clumps in the brain years before symptoms emerge. © 2024 American Association for the Advancement of Science.

Keyword: Parkinsons; Genes & Behavior
Link ID: 29221 - Posted: 03.28.2024

By Elise Cutts In March 2019, on a train headed southwest from Munich, the neuroscientist Maximilian Bothe adjusted his careful grip on the cooler in his lap. It didn’t contain his lunch. Inside was tissue from half a dozen rattlesnake spinal cords packed in ice — a special delivery for his new research adviser Boris Chagnaud, a behavioral neuroscientist based on the other side of the Alps. In his lab at the University of Graz in Austria, Chagnaud maintains a menagerie of aquatic animals that move in unusual ways — from piranhas and catfish that drum air bladders to produce sound to mudskippers that hop around on land on two fins. Chagnaud studies and compares these creatures’ neuronal circuits to understand how new ways of moving might evolve, and Bothe was bringing his rattlesnake spines to join the endeavor. The ways that animals move are just about as myriad as the animal kingdom itself. They walk, run, swim, crawl, fly and slither — and within each of those categories lies a tremendous number of subtly different movement types. A seagull and a hummingbird both have wings, but otherwise their flight techniques and abilities are poles apart. Orcas and piranhas both have tails, but they accomplish very different types of swimming. Even a human walking or running is moving their body in fundamentally different ways. The tempo and type of movements a given animal can perform are set by biological hardware: nerves, muscle and bone whose functions are bound by neurological constraints. For example, vertebrates’ walking tempos are set by circuits in their spines that fire without any conscious input from the brain. The pace of that movement is dictated by the properties of the neuronal circuits that control them. For an animal to evolve a novel way of moving, something in its neurological circuitry has to change. Chagnaud wants to describe exactly how that happens. “In evolution, you don’t just invent the wheel. You take pieces that were already there, and you modify them,” he said. “How do you modify those components that are shared across many different species to make new behaviors?” © 2024 Simons Foundation.

Keyword: Evolution
Link ID: 29194 - Posted: 03.16.2024

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.

Keyword: Pain & Touch
Link ID: 29190 - Posted: 03.16.2024

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

Keyword: Pain & Touch
Link ID: 29187 - Posted: 03.09.2024

By Pam Belluck One of the few treatments the Food and Drug Administration has approved for amyotrophic lateral sclerosis has failed a large clinical trial, and its manufacturer said Friday that it was considering whether to withdraw it from the market. The medication, called Relyvrio, was approved less than two years ago, despite questions about its effectiveness in treating the severe neurological disorder. At the time, the F.D.A.’s reviewers had concluded there was not yet sufficient evidence that the medication could help patients live longer or slow the rate at which they lose functions like muscle control, speaking or breathing without assistance. But the agency decided to greenlight the medication instead of waiting two years for results of a large clinical trial, citing data showing the treatment to be safe and the desperation of patients with a disease that often causes death within two to five years. Since then, about 4,000 patients in the United States have received the treatment, a powder that is mixed with water and either drunk or ingested through a feeding tube and carries a list price of $158,000 a year. Now, results of the 48-week trial of 664 patients are in, and they showed that the treatment did not work better than a placebo. “We are surprised and deeply disappointed,” Justin Klee and Joshua Cohen, the co-chief executive officers of Amylyx Pharmaceuticals, the treatment’s manufacturer, said in a statement. They said they would announce their plans for the medication within eight weeks, “which may include voluntarily withdrawing” it from the market. “We will be led in our decisions by two key principles: doing what is right for people living with A.LS., informed by regulatory authorities and the A.L.S. community, and by what the science tells us,” Mr. Klee and Mr. Cohen said. There are only two other approved A.L.S. medications in the United States: riluzole, approved in 1995, which can extend survival by several months, and edaravone, approved in 2017, which can slow progression by about 33 percent. © 2024 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 29186 - Posted: 03.09.2024