Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

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by Maris Fessenden A new lightweight device with a wisplike tether can record neural activity while mice jump, run and explore their environment. The open-source recording system, which its creators call ONIX, overcomes several of the limitations of previous systems and enables the rodents to move more freely during recording. The behavior that ONIX allows brings to mind children running around in a playground, says Jakob Voigts, a researcher at the Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Virginia, who helped build and test the system. He and his colleagues describe their work in a preprint posted on bioRxiv earlier this month. To understand how the brain creates complex behaviors — such as those found in social interaction, sensory processing and cognition, which are commonly affected in autism — researchers observe brain signals as these behaviors unfold. Head-mounted devices enable researchers to eavesdrop on the electrical chatter between brain cells in mice, rats and primates. But as the smallest of these animal models, mice present some significant challenges. Current neural recording systems are bulky and heavy, making the animals carry up to a fifth of their body weight on their skulls. Predictably, this slows the mice down and tires them out. And most neural recording systems use a tether to relay signals from the mouse’s brain to a computer. But this tether twists and tangles as the mouse turns its head and body, exerting torque that the mouse can feel. Researchers must therefore periodically replace or untangle the tether. Longer tethers allow for more time to elapse between changeouts, but the interruptions still affect natural behavior. And battery-powered, wireless systems add too much weight. Altogether, these challenges inhibit natural behaviors and limit the amount of time that recording can take place, preventing scientists from studying, for example, the complete process of learning a new task. © 2023 Simons Foundation

Keyword: Brain imaging
Link ID: 28930 - Posted: 09.27.2023

By Laura Sanders On a hot, sunny Sunday afternoon in Manhattan, time froze for Jon Nelson. He stood on the sidewalk and said good-bye to his three kids, whose grandfather had come into the city from Long Island to pick them up. Like any parent, Jon is deeply attuned to his children’s quirks. His oldest? Sometimes quiet but bitingly funny. His middle kid? Rates dad a 10 out of 10 on the embarrassment scale and doesn’t need a hug. His 10-year-old son, the baby of the family, is the emotional one. “My youngest son would climb back up into my wife’s womb if he could,” Jon says. “He’s that kid.” An unexpected parade had snarled traffic, so Jon parked illegally along a yellow curb on 36th Street, near where his father-in-law was waiting. It was time to go. His youngest gave the last hug. “He looked up, scared and sad,” Jon says, and asked, “Dad, am I going to see you again?” That question stopped the clock. “I was like, ‘Oh man,’” Jon says. “It was one of those moments where I was living it through his eyes. And I got scared for the first time.” Until that good-bye, Jon hadn’t wanted to live. For years, he had a constant yearning to die — he talks about it like it was an addiction — as he fought deep, debilitating depression. But his son’s question pierced through that heaviness and reached something inside him. “That was the first time I really thought about it. I was like, ‘I kind of hope I don’t die.’ I hadn’t had that feeling in so long.” That hug happened around 5 p.m. on August 21, 2022. Twelve hours later, Jon was wheeled into a surgical suite. There, at Mount Sinai’s hospital just southwest of Central Park, surgery team members screwed Jon’s head into a frame to hold it still. Then they numbed him and drilled two small holes through the top of his skull, one on each side. Through each hole, a surgeon plunged a long, thin wire dotted at the end with electrodes deep into his brain. The wiring, threaded under his skin, snaked around the outside of Jon’s skull and sank down behind his ear. From there, a wire wrapped around to the front, meeting a battery-powered control box that surgeons implanted in his chest, just below his collarbone. © Society for Science & the Public 2000–2023.

Keyword: Depression
Link ID: 28924 - Posted: 09.23.2023

By Phil Jaekl In the mid-1970s, a British researcher named Anthony Barker wanted to measure the speed at which electrical signals travel down the long, slender nerves that can carry signals from the brain to muscles like those in the hand, triggering movement. To find out, he needed a way to stimulate nerves in people. Researchers had already used electrodes placed on the skin to generate a magnetic field that penetrated human tissue — this produced an electric current that activated the peripheral nerves in the limbs. But the technique was painful, burning the skin. Barker, at the University of Sheffield in England, and his colleagues started to work on a better method. In 1985, with promising results under their belts, they tried positioning the coil-shaped magnetic device they’d developed on participants’ heads. The coil emitted rapidly alternating magnetic pulses over the brain region that controls movement, generating weak electrical currents in the brain tissue and activating neurons that control muscles in the hand. After about 20 milliseconds, the participants’ fingers twitched. The technique, now called transcranial magnetic stimulation (TMS), has proved a vital tool for investigating how the human brain works. When targeted to specific brain regions, TMS can temporarily inhibit or enhance various functions – blocking the ability to speak, for instance, or making it easier to commit a series of numbers to memory. And when brain imaging technologies such as functional magnetic resonance imaging (fMRI) emerged in the 1990s, researchers could now “see” inside people’s brains as they received TMS stimulation. They could also observe how neural pathways respond differently to stimulation in psychiatric illnesses like schizophrenia and depression. In recent decades, this fundamental research has yielded new treatments that alter brain activity, with TMS therapies for depression at the fore. In 2008, the US Food and Drug Administration approved NeuroStar, the nation’s first TMS depression device, and many other countries have since sanctioned the approach. Yet even though TMS is now a widely available depression treatment, many questions remain about the method. It’s not clear how long the benefits of TMS can last, for example, or why it appears to work for some people with depression but not others. Another challenge is disentangling the effects of TMS from the placebo effect — when someone believes that they will benefit from treatment and gets better even though they’re receiving a “sham” form of stimulation. © 2023 Annual Reviews

Keyword: Depression
Link ID: 28903 - Posted: 09.10.2023

Neurotransmitters are the words our brain cells use to communicate with one another. For years, researchers relied on tools that provided limited temporal and spatial resolution to track changes in the fast chemical chat between neurons. But that started to change about ten years ago for glutamate—the most abundant excitatory neurotransmitter in vertebrates that plays an essential role in learning, memory, and information processing—when scientists engineered the first glutamate fluorescent reporter, iGluSnFR, which provided a readout of neurons’ fast glutamate release. In 2013, researchers at the Howard Hughes Medical Institute collaborated with scientists from other institutions to develop the first generation of iGluSnFR.1 To create the biosensor, the team combined a bacteria-derived glutamate binding protein, Gltl, a wedged fluorescent GFP protein, and a membrane-targeting protein that anchors the reporter to the surface of the cell. Upon glutamate binding, the Gltl protein changes its conformation, increasing the fluorescence intensity of GFP. In their first study, the team showcased the utility of the biosensor for monitoring glutamate levels by demonstrating selective activation by glutamate in cell cultures. By conducting experiments with brain cells from the C. elegans worm, zebrafish, and mice, they confirmed that the reporter also tracked glutamate in vivo, a finding that set iGluSnFR apart from existing glutamate sensors. The first iGluSnFR generation allowed researchers to study glutamate dynamics in different biological systems, but the indicator could not detect small amounts of the neurotransmitter or keep up with brain cells’ fast glutamate release bouts. Making improvements © 1986–2023 The Scientist.

Keyword: Brain imaging
Link ID: 28901 - Posted: 09.10.2023

By Claudia López Lloreda Cells hidden in the skull may point to a way to detect, diagnose and treat inflamed brains. A detailed look at the skull reveals that bone marrow cells there change and are recruited to the brain after injury, possibly traveling through tiny channels connecting the skull and the outer protective layer of the brain. Paired with the discovery that inflammation in the skull is disease-specific, these new findings collectively suggest the skull’s marrow could serve as a target to track and potentially treat neurological disorders involving brain inflammation, researchers report August 9 in Cell. Immune cells that infiltrate the central nervous system during many diseases and neuronal injury can wreak havoc by flooding the brain with damaging molecules. This influx of immune cells causes inflammation in the brain and spinal cord and can contribute to diseases like multiple sclerosis (SN: 11/26/19). Detecting and dampening this reaction has been an extensive field of research. With this new work, the skull, “something that has been considered as just protective, suddenly becomes a very active site of interaction with the brain, not only responding to brain diseases, but also changing itself in response to brain diseases,” says Gerd Meyer zu Hörste, a neurologist at University of Münster in Germany who was not involved in the study. Ali Ertürk of the Helmholtz Center in Munich and colleagues discovered this potential role for the skull while probing the idea that the cells in skull marrow might behave differently from those in other bones. Ertürk’s team compared the genetic activity of cells in mice skull marrow, and the proteins those cells made, with those in the rodent’s humerus, femur and four other bones, along with the meninges, the protective membranes between the skull and the brain. © Society for Science & the Public 2000–2023.

Keyword: Alzheimers; Multiple Sclerosis
Link ID: 28898 - Posted: 09.07.2023

Jon Hamilton If you've ever had trouble finding your keys or remembering what you had for breakfast, you know that short-term memory is far from perfect. For people who've had a traumatic brain injury (TBI), though, recalling recent events or conversations can be a major struggle. "We have patients whose family cannot leave them alone at home because they will turn on the stove and forget to turn it off," says Dr. Ramon Diaz-Arrastia, who directs the Traumatic Brain Injury Clinical Research Center at the University of Pennsylvania. So Arrastia and a team of scientists have been testing a potential treatment. It involves delivering a pulse of electricity to the brain at just the right time. And it worked in a study of eight people with moderate or severe TBIs, the team reports in the journal Brain Stimulation. A precisely timed pulse to a brain area just behind the ear improved recall by about 20 percent and reduced the person's memory deficit by about half. If the results pan out in a larger study, the approach might improve the lives of many young people who survive a serious TBI, says Diaz-Arrastia, an author of the study and a professor of neurology at Penn. "In many cases, the reason they're unable to rejoin and fully participate in society is because of their memory problems," he says. "And they often have this disability that goes on for many, many decades." But the treatment is not for the timid. It requires patients to have electrodes surgically implanted in their brain. And scientists are still refining the system that delivers the electrical pulses. More than 1.5 million people in the U.S. sustain a TBI each year. Common causes include falls, motor vehicle accidents, assaults, contact sports, and gunshots. © 2023 npr

Keyword: Brain Injury/Concussion
Link ID: 28870 - Posted: 08.09.2023

Max Kozlov Dead in California but alive in New Jersey: that was the status of 13-year-old Jahi McMath after physicians in Oakland, California, declared her brain dead in 2013, after complications from a tonsillectomy. Unhappy with the care that their daughter received and unwilling to remove life support, McMath’s family moved with her to New Jersey, where the law allowed them to lodge a religious objection to the declaration of brain death and keep McMath connected to life-support systems for another four and a half years. Prompted by such legal discrepancies and a growing number of lawsuits around the United States, a group of neurologists, physicians, lawyers and bioethicists is attempting to harmonize state laws surrounding the determination of death. They say that imprecise language in existing laws — as well as research done since the laws were passed — threatens to undermine public confidence in how death is defined worldwide. “It doesn’t really make a lot of sense,” says Ariane Lewis, a neurocritical care clinician at NYU Langone Health in New York City. “Death is something that should be a set, finite thing. It shouldn’t be something that’s left up to interpretation.” Since 2021, a committee in the Uniform Law Commission (ULC), a non-profit organization in Chicago, Illinois, that drafts model legislation for states to adopt, has been revising its recommendation for the legal determination of death. The drafting committee hopes to clarify the definition of brain death, determine whether consent is required to test for it, specify how to handle family objections and provide guidance on how to incorporate future changes to medical standards. The broader membership of the ULC will offer feedback on the first draft of the revised law at a meeting on 26 July. After members vote on it, the text could be ready for state legislatures to consider by the middle of next year. But as the ULC revision process has progressed, clinicians who were once eager to address these issues have become increasingly worried. © 2023 Springer Nature Limited

Keyword: Consciousness
Link ID: 28853 - Posted: 07.22.2023

By Stephanie Pappas Have you felt butterflies in your stomach or hunger pangs? Those “gut feelings” happen thanks to the vagus nerve, which is a superhighway that connects the brain and the gut. In recent years the vagus nerve has become an intriguing target for researchers looking to cure disorders of both the brain and the body. Vagus nerve stimulation—usually achieved with an electrode implanted in the neck to deliver electrical pulses directly to the nerve—is an approved treatment for epilepsy and some forms of depression. Scientists are now studying vagus nerve stimulation (VNS) for disorders such as rheumatoid arthritis and the inflammatory bowel disease Crohn’s. What gives this nerve such widespread impact? The vagus nerve is the longest of the cranial nerves, which emerge directly from the brain rather than traveling through the spinal cord. It begins at an opening at the base of the skull and runs down the neck and into the abdomen, where it collects signals from the viscera and helps regulate the automatic processes of the body, from digestion to sleep to inflammation. About 80 percent of its signals are sensory ones that travel from the inner organs up to the brain, while the other 20 percent travel from the brain to the body and regulate things such as intestinal contractions and heart rate. The vagus nerve is the key player in the parasympathetic nervous system, which is the “rest and digest” system that calms the body during times of low stress. “If you are relaxed, if you are sleeping, if you are in a restorative phase, it’s the vagus nerve dominating,” says Gregor Hasler, a psychiatrist at the University of Fribourg in Switzerland, who has written about the gut-brain connection.

Keyword: Depression; Epilepsy
Link ID: 28843 - Posted: 07.06.2023

Nicola Davis Science correspondent Researchers have discovered a genetic variant that appears to influence the speed at which multiple sclerosis (MS) progresses, potentially paving the way for new treatments. According to the MS International Federation, about 2.9 million people worldwide have MS, a condition in which the insulating coating of the nerves in the brain and spinal cord is damaged by the immune system. The nerve fibres themselves can also become damaged. While some people have a relapsing remitting form of the disease, others experience gradual progression that in some can cause severe disability. Researchers say they have identified a genetic variant that appears to increase the severity of the disease. They found that people who inherit the variant from both parents need a walking aid almost four years sooner than those without. “This is a very substantial effect for a single genetic variant,” said Sergio Baranzini, a professor of neurology at the University of California, San Francisco and co-senior author of the study. “Furthermore, this variant affects genes that are active in the central nervous system, a clear contrast to variants that confer risk [of MS], which overwhelmingly affect the immune system.” The study, published in the journal Nature, was an international endeavour, involving 70 institutions around the world. To make their discovery, the team analysed genetic data from more than 12,000 people with MS, screening more than 7m genetic variants for associations with the speed of disease progression. The team found that one variant, nestled between two genes called DYSF and ZNF638, was associated with a more rapid increase in disability. © 2023 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28840 - Posted: 07.01.2023

Emily Waltz Researchers have been exploring whether zapping a person’s brain with electrical current through electrodes on their scalp can improve cognition.Credit: J.M. Eddin/Military Collection/Alamy After years of debate over whether non-invasively zapping the brain with electrical current can improve a person’s mental functioning, a massive analysis of past studies offers an answer: probably. But some question that conclusion, saying that the analysis spans experiments that are too disparate to offer a solid answer. In the past six years, the number of studies testing the therapeutic effects of a class of techniques called transcranial electrical stimulation has skyrocketed. These therapies deliver a painless, weak electrical current to the brain through electrodes placed externally on the scalp. The goal is to excite, disrupt or synchronize signals in the brain to improve function. Researchers have tested transcranial alternating current stimulation (tACS) and its sister technology, tDCS (transcranial direct current stimulation), on both healthy volunteers and those with neuropsychiatric conditions, such as depression, Parkinson’s disease or addiction. But study results have been conflicting or couldn’t be replicated, leading researchers to question the efficacy of the tools. The authors of the new analysis, led by Robert Reinhart, director of the cognitive and clinical neuroscience laboratory at Boston University in Massachusetts, say they compiled the report to quantify whether tACS shows promise, by comparing more than 100 studies of the technique, which applies an oscillating current to the brain. “We have to address whether or not this technique is actually working, because in the literature, you have a lot of conflicting findings,” says Shrey Grover, a cognitive neuroscientist at Boston University and an author on the paper. © 2023 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 28807 - Posted: 05.31.2023

By Scientific American Custom Media Megan Hall: How does the stomach tell the brain it’s full? How do cells in our body grow and divide? James Rothman realized that the fundamental biology behind these processes are basically the same. In 2010, he shared The Kavli Prize in Neuroscience with Richard Scheller and Thomas Südhof for their work detailing how nerve cells communicate with each other on a microscopic level. Three years later, he received the Nobel Prize. Hall: James Rothman was pleasantly surprised when he received The Kavli Prize in Neuroscience. James Rothman: I'd always thought of myself as a biochemist first and a cell biologist second. And I never really thought of myself as a neuroscientist. Hall: He did apply to a neuroscience program in grad school… Rothman: It all just made a whole lot of sense, except for the fact that I wasn't admitted. Hall: But James is not the kind of person to worry about labels. In fact, he’s explored a range of scientific disciplines. As an undergrad at Yale, he studied physics, maybe in part because he grew up in the 50s. Rothman: Scientists and doctors were really the most admired in the 1950s. And it was the physicists in particular. Einstein, Oppenheimer, people like that. Hall: But his father worried about his career options, so he convinced James to try a biology course. Rothman: And I just fell in love. Hall: So, he ditched physics and decided to go to Harvard Medical School to learn more about biology. Rothman: In the end I never finished medical school. Hall: But, while he was there, he stumbled upon his life’s work. Rothman: I was a first-year medical student and I was listening to a lecture in our course on histology and cell biology. Hall: The professor was showing images that had been captured by scientists only a few decades before. They showed, for the first time, how complex the cell is. Rothman: The cell is not just, like a dumb little liquid inside. It's a highly organized place. It's more like a city than anything else. © 2023 Scientific American,

Keyword: Biomechanics
Link ID: 28805 - Posted: 05.31.2023

By Emily Underwood It’s a classic science fiction trope: Astronauts on an interstellar journey are kept in sleek, refrigerated pods in a state of suspended animation. Although such pods remain purely fictional, scientists have pursued research into inducing a hibernation-like state in humans to lessen the damage caused by medical conditions such as heart attacks and stroke, and to reduce the stress and costs of future long-distance space sojourns. In a study published today in Nature Metabolism, scientists report that they can trigger a similar state in mice by targeting part of their brain with pulses of ultrasound. Some experts are calling it a major technical step toward achieving this feat in humans, whereas others say it’s a stretch to extrapolate the results to our species. "It’s an amazing paper,” says Frank van Breukelen, a biologist who studies hibernation at the University of Nevada, Las Vegas and co-authored an editorial accompanying the study. The work builds on a flurry of recent studies that pinpoint specific populations of neurons in a region called the preoptic area (POA) of the hypothalamus. These cells act like an on-off switch for “torpor”—a sluggish, energy-saving state the animals enter when they’re dangerously cold or malnourished. In previous studies, scientists genetically engineered these neurons to respond to light or certain chemicals, and found they could cause mice to enter a torpid state even when they were warm and well-fed. Such invasive techniques can’t be easily translated to people, however, Breukelen notes. “That’s really not going to happen in people.” The new ultrasound study, led by bioengineer Hong Chen and her team at Washington University in St. Louis required no genetic engineering. Chen knew from previous research that some neurons have specialized pores called TRPM2 ion channels that change shape in response to ultrasonic waves, including the subset of POA cells that controls mouse torpor. To see what effect that had on the animals’ behavior, her team next glued miniature, speakerlike devices on the heads of mice to focus these waves on the POA.

Keyword: Sleep; Brain imaging
Link ID: 28800 - Posted: 05.27.2023

John Katsaras Charles Patrick Collier Dima Bolmatov Your brain is responsible for controlling most of your body’s activities. Its information processing capabilities are what allow you to learn, and it is the central repository of your memories. But how is memory formed, and where is it located in the brain? Although neuroscientists have identified different regions of the brain where memories are stored, such as the hippocampus in the middle of the brain, the neocortex in the top layer of the brain and the cerebellum at the base of the skull, they have yet to identify the specific molecular structures within those areas involved in memory and learning. Research from our team of biophysicists, physical chemists and materials scientists suggests that memory might be located in the membranes of neurons. Neurons are the fundamental working units of the brain. They are designed to transmit information to other cells, enabling the body to function. The junction between two neurons, called a synapse, and the chemistry that takes place between synapses, in the space called the synaptic cleft, are responsible for learning and memory. At a more fundamental level, the synapse is made of two membranes: one associated with the presynaptic neuron that transmits information, and one associated with the postsynaptic neuron that receives information. Each membrane is made up of a lipid bilayer containing proteins and other biomolecules. The changes taking place between these two membranes, commonly known as synaptic plasticity, are the primary mechanism for learning and memory. These include changes to the amounts of different proteins in the membranes, as well as the structure of the membranes themselves.

Keyword: Learning & Memory
Link ID: 28777 - Posted: 05.10.2023

By Geoffrey Giller From the brightly colored poison frogs of South America to the prehistoric-looking newts of the Western US, the world is filled with beautiful, deadly amphibians. Just a few milligrams of the newt’s tetrodotoxin can be fatal, and some of those frogs make the most potent poisons found in nature. In recent years, scientists have become increasingly interested in studying poisonous amphibians and are starting to unravel the mysteries they hold. How is it, for example, that the animals don’t poison themselves along with their would-be predators? And how exactly do the ones that ingest toxins in order to make themselves poisonous move those toxins from their stomachs to their skin? Even the source of the poison is sometimes unclear. While some amphibians get their toxins from their diet, and many poisonous organisms get theirs from symbiotic bacteria living on their skin, still others may or may not make the toxins themselves — which has led scientists to rethink some classic hypotheses. Over the long arc of evolution, animals have often turned to poisons as a means of defense. Unlike venoms — which are injected via fang, stinger, barb, or some other specialized structure for offensive or defensive purposes — poisons are generally defensive toxins a creature makes that must be ingested or absorbed before they take effect. Amphibians tend to store their poisons in or on their skin, presumably to increase the likelihood that a potential predator is deterred or incapacitated before it can eat or grievously wound them. Many of their most powerful toxins — like tetrodotoxin, epibatidine and the bufotoxins originally found in toads — are poisons that interfere with proteins in cells, or mimic key signaling molecules, thus disrupting normal function. © 2023 Annual Reviews

Keyword: Neurotoxins
Link ID: 28757 - Posted: 04.29.2023

By Jake Buehler Shimmering, gelatinous comb jellies wouldn’t appear to have much to hide. But their mostly see-through bodies cloak a nervous system unlike that of any other known animal, researchers report in the April 21 Science. In the nervous systems of everything from anemones to aardvarks, electrical impulses pass between nerve cells, allowing for signals to move from one cell to the next. But the ctenophores’ cobweb of neurons, called a nerve net, is missing these distinct connection spots, or synapses. Instead, the nerve net is fused together, with long, stringy neurons sharing a cell membrane, a new 3-D map of its structure shows. While the nerve net has been described before, no one had generated a high-resolution, detailed picture of it. It’s possible the bizarre tissue represents a second, independent evolutionary origin of a nervous system, say Pawel Burkhardt, a comparative neurobiologist at the University of Bergen in Norway, and colleagues. Superficially similar to jellyfish, ctenophores are often called comb jellies because they swim using rows of beating, hairlike combs. The enigmatic phylum is considered one of the earliest to branch off the animal tree of life. So ctenophores’ possession of a simple nervous system has been of particular interest to scientists interested in how such systems evolved. Previous genetics research had hinted at the strangeness of the ctenophore nervous system. For instance, a 2018 study couldn’t find a cell type in ctenophores with a genetic signature that corresponded to recognizable neurons, Burkhardt says. Burkhardt, along with neurobiologist Maike Kittelmann of Oxford Brookes University in England and colleagues, examined young sea walnuts (Mnemiopsis leidyi) using electron microscopes, compiling many images to reconstruct the entire net structure. Their 3-D map of a 1-day-old sea walnut revealed the funky synapse-free fusion between the five sprawling neurons that made up the tiny ctenophore’s net. © Society for Science & the Public 2000–2023.

Keyword: Evolution
Link ID: 28745 - Posted: 04.22.2023

Miryam Naddaf Virtual models representing the brains of people with epilepsy could help to enable more-effective treatments of the disease by showing neurosurgeons precisely which zones are responsible for seizures. The models, created using a computational system known as the Virtual Epileptic Patient (VEP), have been developed as part of the Human Brain Project (HBP), a ten-year European initiative focused on digital brain research. The approach is being tested in a clinical trial called EPINOV, to evaluate whether it improves the success rate of epilepsy surgery. “It’s an example of personalized medicine,” says Aswin Chari, a neurosurgeon at University College London. VEP uses “the patient’s own brain scans [and] the patient’s own brainwave-recording data to build a model and improve our understanding of where their seizures are coming from”. Life-changing surgery Epileptic seizures are brought on by abnormal brain activity, and around one-third of the 50 million people living with epilepsy worldwide do not respond to anti-seizure drugs. “For those people, surgery is a huge game changer,” says Chari. It aims to free patients from seizures by removing parts of the epileptogenic zone — the brain region that is thought to initiate seizures. To identify the epileptogenic zone, clinicians currently use scanning techniques such as magnetic resonance imaging (MRI) and electroencephalogram (EEG) to investigate brain activity. They also perform stereoelectroencephalography (SEEG), which involves placing up to 16 electrodes, each 7 centimetres long, through the skull to monitor the activity of specific areas for 1–2 weeks. © 2023 Springer Nature Limited

Keyword: Epilepsy; Brain imaging
Link ID: 28732 - Posted: 04.09.2023

By Nora Bradford For the first time, scientists have recorded brain waves from freely moving octopuses. The data reveal some unexpected patterns, though it’s too early to know how octopus brains control the animals’ behavior, researchers report February 23 in Current Biology. “Historically, it’s been so hard to do any recordings from octopuses, even if they’re sedated,” says neuroscientist Robyn Crook of San Francisco State University, who was not involved in the study. “Even when their arms are not moving, their whole body is very pliable,” making attaching recording equipment tricky. Octopuses also tend to be feisty and clever. That means they don’t usually put up with the uncomfortable equipment typically used to record brain waves in animals, says neuroethologist Tamar Gutnick of the University of Naples Federico II in Italy. To work around these obstacles, Gutnick and colleagues adapted portable data loggers typically used on birds, and surgically inserted the devices into three octopuses. The researchers also placed recording electrodes inside areas of the octopus brain that deal with learning and memory. The team then recorded the octopuses for 12 hours while the cephalopods went about their daily lives — sleeping, swimming and self-grooming — in tanks. Some brain wave patterns emerged across all three octopuses in the 12-hour period. For instance, some waves resembled activity in the human hippocampus, which plays a crucial role in memory consolidation. Other brain waves were similar to those controlling sleep-wake cycles in other animals. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28716 - Posted: 03.25.2023

Jon Hamilton Mora Leeb places some pieces into a puzzle during a local puzzle tournament. The 15-year-old has grown up without the left side of her brain after it was removed when she was very young. Seth Leeb In most people, speech and language live in the brain's left hemisphere. Mora Leeb is not most people. When she was 9 months old, surgeons removed the left side of her brain. Yet at 15, Mora plays soccer, tells jokes, gets her nails done, and, in many ways, lives the life of a typical teenager. "I can be described as a glass-half-full girl," she says, pronouncing each word carefully and without inflection. Her slow, cadence-free speech is one sign of a brain that has had to reorganize its language circuits. Yet to a remarkable degree, Mora's right hemisphere has taken on jobs usually done on the left side. It's an extreme version of brain plasticity, the process that allows a brain to modify its connections to adapt to new circumstances. Brain plasticity is thought to underlie learning, memory, and early childhood development. It's also how the brain revises its circuitry to help recover from a brain injury — or, in Mora's case, the loss of an entire hemisphere. Scientists hope that by understanding the brains of people like Mora, they can find ways to help others recover from a stroke or traumatic brain injury. They also hope to gain a better understanding of why very young brains are so plastic. Sometime in the third trimester of Ann Leeb's pregnancy, the child she was carrying had a massive stroke on the left side of her brain. No one knew it at the time. © 2023 npr

Keyword: Development of the Brain; Epilepsy
Link ID: 28714 - Posted: 03.23.2023

By Lisa Sanders, M.D. “It’s happening,” the 58-year-old man said quietly. Dr. Mark Chelmowski looked over to observe his patient. He was leaning forward, elbows on table, head propped up on his hands. Beads of sweat suddenly appeared on the man’s brow. More popped up on his cheeks, then his jaw. Rivulets ran down the contours of his face, then dripped off his chin onto the table. The man’s eyes were closed. He almost seemed asleep. Chelmowski said his name. “Yes, doctor” was the only response the normally chatty man gave. It was as if he were somehow distracted by the profound sweating. The patient’s vital signs were normal. He didn’t have a fever. His blood pressure and heart rate were normal. Throughout the exam, the patient sat quietly sweating. The collar, front and back of his shirt darkened. Then, as abruptly as it started, it was over. He opened his eyes and looked at Chelmowski. The patient could see the surprise in his doctor’s face. Chelmowski knew about his episodes of sweating — the two of them had been trying to figure them out for the past five months — but he had not yet witnessed one. The first time it happened, the patient was in his car on the way to the gym when suddenly he felt intensely hot. It was a bright July day in the Milwaukee area and seasonably warm. But this heat felt as if it came from inside his body. A vague prickling sensation spread down his face and neck to his chest and back. His heart seemed to speed up and then — pow — he was drenched in sweat. He turned the car around and headed home. He was describing the strange event to his partner when it happened again. And again. Each episode lasted only a couple of minutes, but it was strange. The sweating was so excessive. After a fourth episode, the patient’s partner insisted they go to the emergency room. He had another bout in front of the E.R. doctor, who immediately admitted him to the hospital. He was worried the patient might be having a heart attack. Profuse sweating often accompanies myocardial infarctions, the doctor told him. But it wasn’t his heart. He was discharged the next day and encouraged to follow up with his primary-care doctor. © 2023 The New York Times Company

Keyword: Epilepsy; Hormones & Behavior
Link ID: 28696 - Posted: 03.11.2023

by Laura Dattaro Neurons deep in the prefrontal cortex of fragile X model mice have trouble generating the electrical spikes needed to transmit information, according to a new study. The difficulty originates from faulty sodium channels. Fragile X syndrome, one of the leading genetic causes of autism, results from mutations in the gene FMR1. People with the condition often have difficulty with executive-function skills, such as working memory and planning. The new study may explain why, says Randi Hagerman, medical director of the MIND Institute at the University of California, Davis: The disruption to signals propagating through the prefrontal cortex may impede the region’s role in coordinating communication among other parts of the brain. Some drugs that regulate sodium channels, such as the diabetes drug metformin, are already approved for use in people. “This is a great animal model to look at the effects of medication,” says Hagerman, who was not involved in the new work. Mutations in the autism-linked gene SCN2A, which encodes a protein for the sodium channel Nav1.2, also suppress dendritic spikes, researchers previously showed in mice. The cellular mechanism for channel disruption is different between the models, but it’s possible that multiple genetic causes of autism “coalesce around sodium channel disfunction,” says Darrin Brager, research associate professor of neuroscience at the University of Texas at Austin and lead investigator on the FMR1 study. “The same channel is altered, and that’s changing the way the cells are able to integrate information and transmit it.” © 2023 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 28677 - Posted: 02.22.2023