Chapter 3. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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By Claudia López Lloreda Learning lots of new information as a baby requires a pool of ready-to-go, immature connections between nerve cells to form memories quickly. Called silent synapses, these connections are inactive until summoned to help create memories, and were thought to be present mainly in the developing brain and die off with time. But a new study reveals that there are many silent synapses in the adult mouse brain, researchers report November 30 in Nature. Neuroscientists have long puzzled over how the adult human brain can have stable, long-term memories, while at the same time maintaining a certain flexibility to be able to make new memories, a concept known as plasticity (SN: 7/27/12). These silent synapses may be part of the answer, says Jesper Sjöström, a neuroscientist at McGill University in Montreal who was not involved with the study. “The silent synapses are ready to hook up,” he says, possibly making it easier to store new memories as an adult by using these connections instead of having to override or destabilize mature synapses already connected to memories. “That means that there’s much more room for plasticity in the mature brain than we previously thought.” In a previous study, neuroscientist Mark Harnett of MIT and his colleagues had spotted many long, rod-shaped structures called filopodia in adult mouse brains. That surprised Harnett because these protrusions are mostly found on nerve cells in the developing brain. “Here they were in adult animals, and we could see them crystal clearly,” Harnett says. So he and his team decided to examine the filopodia to see what role they play, and if they were possibly silent synapses. The researchers used a technique to expand the brains of adult mice combined with high-resolution microscopy. Since nerve cell connections and the molecules called receptors that allow for communication between connected cells are so small, these methods revealed synapses that past research missed. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory
Link ID: 28602 - Posted: 12.17.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28580 - Posted: 12.03.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28579 - Posted: 12.03.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022

By Erika Check Hayden Weeks after Valeria Schenkel took an experimental drug named after her, the daily seizures that had afflicted her from birth became less frequent. But the drug caused fluid to build up in her brain, and a year later, she died at age 3. The drug was given to only one other child, and she experienced the same side effect and nearly died last year. The drug contained snippets of genetic material tailor-made to turn off the mutated gene causing the extremely rare form of epilepsy that these children were born with. A handful of researchers and nonprofit organizations have raised millions of dollars to make these treatments, known as antisense drugs, for at least 19 children and adults with severe diseases that are too rare to garner interest from pharmaceutical companies. The treatments have helped some of these patients, raising hopes that the personalized approach might one day save thousands of lives. But the brain side effect, known as hydrocephalus, reported on Sunday at the American Neurological Association meeting in Chicago, is a blow for the niche medical field that has made rapid progress over the past five years. Hydrocephalus happens when too much fluid fills cavities in the brain, increasing pressure on brain tissue and risking lethal damage if untreated. “I think it’s worth saying: No question that encountering hydrocephalus has been a setback, sobering and important,” said Dr. Timothy Yu, the neurologist and genetics researcher at Boston Children’s Hospital who developed the drug, known as valeriasen. But traditional drug companies, he added, are not helping patients with thousands of rare, untreatable and rapidly progressing diseases that cause death and severe disabilities. Personalized genetic treatments may be their only hope. “We have to learn as much as we can from each and every one, because they’re just so incredibly valuable in every sense,” Dr. Yu said. Scientists first imagined creating “antisense oligonucleotide” drugs — pieces of custom-made DNA or RNA designed to correct for genetic errors in cells — in the 1960s. But it took decades to make stable and effective versions of such drugs. © 2022 The New York Times Company

Keyword: Epilepsy; Development of the Brain
Link ID: 28529 - Posted: 10.28.2022

By Sandra G. Boodman For years Carter Caldwell had adamantly rejected doctors’ recommendations that he consider surgery to treat the frequent, uncontrolled seizures that were ravaging his brain. Caldwell, who had developed epilepsy when he was 28, regarded the operation that involved removing a portion of his brain as too big a risk — particularly because doctors weren’t sure what was causing the seizures and couldn’t pinpoint their location. Instead the Philadelphia business executive had organized his life to minimize certain foreseeable hazards: He lived downtown and didn’t drive. He didn’t push his toddler’s stroller. When taking the train he stood at the back of the platform — nowhere near the tracks in case he suddenly collapsed. His colleagues at work knew about his condition. But that calculus changed abruptly in November 2014. Caldwell, accompanied by his wife, Connie, and their 3-year-old son, was atop a hill at Pennsylvania’s Valley Forge National Historical Park posing for photos for a holiday card. Without warning he began an awkward shuffling walk that signified the onset of a seizure. Then he lost consciousness and fell head first down a rocky 15-foot embankment before landing at the edge of a stream. “Thankfully,” he said, “I didn’t roll into the stream.” He spent the next 2 1/2 weeks in a nearby hospital where a plastic surgeon performed multiple operations on his broken jawbone, lacerated cheek and shattered eye socket. “I remember him saying, ‘I can’t believe this happened in front of my family,’ ” recalled his longtime neurologist John R. Pollard, formerly associate director of the epilepsy center at the University of Pennsylvania. Pollard had warned Caldwell that his intractable seizures, which had proved resistant to numerous medications, placed him at risk for sudden death or serious injury. In September 2015 a successful operation unmasked the very unusual cause of Caldwell’s seizures, a culprit experts had long suspected but had been unable to definitively identify.

Keyword: Epilepsy; Emotions
Link ID: 28518 - Posted: 10.19.2022

By Lisa Sanders, M.D. “What just happened?” The 16-year-old girl’s voice was flat and tired. “I think you had a seizure,” her mother answered. Her daughter had asked to be taken to the pediatrician’s office because she hadn’t felt right for the past several weeks — not since she had what looked like a seizure at school. And now she’d had another. “You’re OK now,” the mother continued. “It’s good news because it means that maybe we finally figured out what’s going on.” To most people, that might have been a stretch — to call having a seizure good news. But for the past several years, the young woman had been plagued by headaches, episodes of dizziness and odd bouts of profound fatigue, and her mother embraced the possibility of a treatable disorder. The specialists she had taken her daughter to see attributed her collection of symptoms to the lingering effect of the many concussions she suffered playing sports. She had at least one concussion every year since she was in the fourth grade. Because of her frequent head injuries, her parents made her drop all her sports. Even when not on the playing field, the young woman continued to fall and hit her head. The headaches and other symptoms persisted long after each injury. She saw several specialists who agreed that she had what was called persistent post-concussive syndrome — symptoms caused either by a severe brain injury or, in her case, repeated mild injuries. She should get better with time and patience, the girl and her mother were told. And yet her head pounded and she retreated to her darkened room several times a week. She did everything her doctors suggested: She got plenty of sleep, rested when she was tired and tried to be patient. But she still got headaches, still got dizzy. She found it harder and harder to pay attention. For the past couple of years, it had even started to affect her grades. © 2022 The New York Times Company

Keyword: Epilepsy; Attention
Link ID: 28514 - Posted: 10.15.2022

James Brunton Badenoch Monkeypox’s effect on the skin – the disfiguring rashes – and the flu-like symptoms have been well described, but few have investigated the neurological and psychiatric problems the virus might cause. There are historic reports of neurological complications in people infected with the related smallpox virus and in people vaccinated against smallpox, which contains the related vaccinia virus. So my colleagues and I wanted to know whether monkeypox causes similar problems. We looked at all the evidence from before the current monkeypox pandemic of neurological or psychiatric problems in people with a monkeypox infection. The results are published in the journal eClinicalMedicine. A small but noticeable proportion of people (2% to 3%) with monkeypox became very unwell and developed serious neurological problems, including seizure and encephalitis (inflammation of the brain that can cause long-term disability). We also found that confusion occurred in a similar number of people. It’s important to note, though, that these figures are based on a few studies with few participants. Besides the severe and rare brain problems, we found evidence of a broader group of people with monkeypox who had more common neurological symptoms including headache, muscle ache and fatigue. From looking at the studies, it was unclear how severe these symptoms were and how long they lasted. It was also unclear how many people with monkeypox had psychiatric problems - such as anxiety and depression - as few studies looked into it. Of those that did, low mood was frequently reported.. © 2010–2022, The Conversation US, Inc.

Keyword: Epilepsy; Learning & Memory
Link ID: 28475 - Posted: 09.14.2022

By Kurt Kleiner The human brain is an amazing computing machine. Weighing only three pounds or so, it can process information a thousand times faster than the fastest supercomputer, store a thousand times more information than a powerful laptop, and do it all using no more energy than a 20-watt lightbulb. Researchers are trying to replicate this success using soft, flexible organic materials that can operate like biological neurons and someday might even be able to interconnect with them. Eventually, soft “neuromorphic” computer chips could be implanted directly into the brain, allowing people to control an artificial arm or a computer monitor simply by thinking about it. Like real neurons — but unlike conventional computer chips — these new devices can send and receive both chemical and electrical signals. “Your brain works with chemicals, with neurotransmitters like dopamine and serotonin. Our materials are able to interact electrochemically with them,” says Alberto Salleo, a materials scientist at Stanford University who wrote about the potential for organic neuromorphic devices in the 2021 Annual Review of Materials Research. Salleo and other researchers have created electronic devices using these soft organic materials that can act like transistors (which amplify and switch electrical signals) and memory cells (which store information) and other basic electronic components. The work grows out of an increasing interest in neuromorphic computer circuits that mimic how human neural connections, or synapses, work. These circuits, whether made of silicon, metal or organic materials, work less like those in digital computers and more like the networks of neurons in the human brain. © 2022 Annual Reviews

Keyword: Robotics; Learning & Memory
Link ID: 28449 - Posted: 08.27.2022

Diana Kwon People’s ability to remember fades with age — but one day, researchers might be able to use a simple, drug-free method to buck this trend. In a study published on 22 August in Nature Neuroscience1, Robert Reinhart, a cognitive neuroscientist at Boston University in Massachusetts, and his colleagues demonstrate that zapping the brains of adults aged over 65 with weak electrical currents repeatedly over several days led to memory improvements that persisted for up to a month. Previous studies have suggested that long-term memory and ‘working’ memory, which allows the brain to store information temporarily, are controlled by distinct mechanisms and parts of the brain. Drawing on this research, the team showed that stimulating the dorsolateral prefrontal cortex — a region near the front of the brain — with high-frequency electrical currents improved long-term memory, whereas stimulating the inferior parietal lobe, which is further back in the brain, with low-frequency electrical currents boosted working memory. “Their results look very promising,” says Ines Violante, a neuroscientist at the University of Surrey in Guildford, UK. “They really took advantage of the cumulative knowledge within the field.” Using a non-invasive method of stimulating the brain known as transcranial alternating current stimulation (tACS), which delivers electrical currents through electrodes on the surface of the scalp, Reinhart’s team conducted a series of experiments on 150 people aged between 65 and 88. Participants carried out a memory task in which they were asked to recall lists of 20 words that were read aloud by an experimenter. The participants underwent tACS for the entire duration of the task, which took 20 minutes. © 2022 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 28445 - Posted: 08.24.2022

By Erin Garcia de Jesús As Tanina Agosto went through her normal morning routine in July 2007, she realized something was wrong. The 29-year-old couldn’t control her left side, even her face. “Literally the top of my head to the bottom of my foot on the left side of my body could not feel anything.” The next day, Agosto spoke with a doctor at the New York City hospital where she works as a medical secretary. He told her that she probably had a pinched nerve and to see a chiropractor. But chiropractic care didn’t help. Months later, Agosto needed a cane to get around, and moving her left leg and arm required lots of concentration. She couldn’t work. Numbness and tingling made cooking and cleaning difficult. It felt a bit like looping a rubber band tightly around a finger until it loses sensation, Agosto says. Once the rubber band comes off, the finger tingles for a bit. But for her, the tingling wouldn’t stop. Finally, she recalls, one chiropractor told her, “I’m not too big of a person to say there’s something very wrong with you, and I don’t know what it is. You need to see a neurologist.” In November 2008, tests confirmed that Agosto had multiple sclerosis. Her immune system was attacking her brain and spinal cord. Agosto knew nothing about MS except that a friend of her mother’s had it. “At the time, I was like, there’s no way I’ve got this old lady’s condition,” she says. “To be hit with that and know that there’s no cure — that was just devastating.” Why people develop the autoimmune disorder has been a long-standing question. Studies have pointed to certain gene variations and environmental factors. For decades, a common virus called Epstein-Barr virus has also been high on the list of culprits. © Society for Science & the Public 2000–2022.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28428 - Posted: 08.11.2022

Mo Costandi We spend approximately one-third of our lives sleeping, but why sleep is important is a big unanswered question, one which science has only begun to answer recently. We now know, for example, that the brain cleans itself while we sleep, and that long-term memories form during the rapid eye movement (REM) stage of sleep. Your brain is highly active during sleep Sleep can be defined as a temporary state of unconsciousness, during which our responses to the outside world are reduced. Yet, we also know that the brain is active during sleep, and there is growing evidence that it remains highly responsive: For instance, your sleeping brain will respond to your name, categorize words and then prepare appropriate actions, and even learn new information. Now, a new study by researchers at UCLA and Tel Aviv University shows that the human brain remains highly responsive to sound during sleep, but it does not receive feedback from higher order areas — sort of like an orchestra with “the conductor missing.” The findings could point to a better understanding of the extent to which the brain processes information in disorders of consciousness such as coma and vegetative states, and to the neural mechanisms of conscious awareness. The missing conductor Hanna Hayat and her colleagues had the rare opportunity to record the activity of cells directly from the brains of 13 patients with drug-resistant epilepsy, who were being evaluated for brain surgery and gave written consent to participate in the study during the evaluation. The researchers implanted depth electrodes in multiple regions of the patients’ brains, primarily to identify the source of their seizures, so that the abnormal tissue could be surgically removed. Over the course of eight overnight sessions and six daytime naps, they played various sounds — including words, sentences and music — to the patients through bedside loudspeakers. They also used standard electroencephalogram (EEG) to monitor the patients’ sleep stages and recorded their sleep behavior with video. © Copyright 2007-2022 & BIG THINK,

Keyword: Sleep
Link ID: 28416 - Posted: 08.03.2022

By Hilary Achauer I sat in a dark room, eyes closed, with a device strapped to my head that looked like a futuristic bike helmet. For 10 minutes, while I concentrated on not accidentally opening my eyes, the prongs sticking out of this gadget and onto my scalp measured a health marker I never thought to assess: my cognitive health. When I booked my brain wave recording (also known as electroencephalography, or EEG), I expected to pull up to an office park with medical clinic vibes, but instead my GPS led me to an ocean-view storefront decorated like a cross between a surf shop and a luxury spa, with a sign in the window promising “Mental Wellness, Reimagined.” Located in Cardiff-by-the-Sea, a wealthy coastal town north of San Diego, Wave Neuroscience promises to help your brain perform better with a noninvasive treatment that uses magnets on the brain. We’re talking mental clarity, improved focus and concentration, and even a shift in mood. As a 48-year-old whose work requires focus and creativity, I was intrigued, but also nervous. Should I mess with a brain that, while not perfect, functions reasonably well? Advertisement Getting the EEG, which costs $100, was like meditating with a device strapped to my head, but it was more relaxing than that sounds. The tech gave me periodic updates, letting me know how much time had elapsed, and afterward I was ushered into an office where I met with Alexander Ring, director of applied science at Wave Neuroscience, via Zoom. Together we reviewed my “braincare report,” a one-page analysis generated in five minutes, comparing my brain waves with Wave Neuroscience’s database of tens of thousands of EEGs. Ring said my brain was generally performing well and that I showed cognitive flexibility and a capability to focus under pressure, but that I had a little bit more theta activity, or slow brain waves, than they normally like to see. He also pointed out a slight frequency mismatch between the back and front of my brain, which might affect my concentration and cause me to have to reread a paragraph to absorb the information. Rude, but accurate. © 2022 The Slate Group LLC. All rights reserved.

Keyword: Brain imaging; Attention
Link ID: 28347 - Posted: 06.01.2022

By Peter Kendall As he gets ready for sleep each night, Don Tucker slips on an electrode cap and checks a little computer on his bedside table. Many workers at the private lab, run by the professor emeritus at the University of Oregon, follow the same routine. The experimental device monitors the nightly voyage through sleep. After sensing light sleep for a few minutes, it pulses electric current through the scalp and skull, nudging the brain into that nirvana known as deep sleep. The goal is not just a more restful slumber. Groundbreaking discoveries made in the past decade have revealed that the brain has a power-washing system that switches into high gear during deep sleep, flushing away harmful waste. This nightly cleanup is part of the restorative power of sleep and revives concentration, memory and motor skills. As we age, however, this cleansing system gets sloppier, and it can begin to leave behind some of the metabolic detritus of the day, including the amyloid beta proteins found in the plaque that characterize Alzheimer’s disease and other devastating neurological disorders. The controversial approval of an Alzheimer’s drug reignites the battle over the underlying cause of the disease The stunning revelation in 2012 of this previously unknown brain infrastructure — dubbed the glymphatic system — has ushered in a new age of research and invention not only about sleep but also aging, dementia and brain injury. Nearly 300 research papers were published last year on the glymphatic system. © 1996-2022 The Washington Post

Keyword: Sleep
Link ID: 28346 - Posted: 06.01.2022

by Niko McCarty A new miniature, head-mounted microscope can simultaneously record the activity of thousands of neurons at different depths within the brains of freely moving mice. The smallest functional two-photon microscope to date, it can image neurons almost anywhere in the brain, with subcellular resolution. The device, called MINI2P (miniature two-photon microscope), can also collect data from the same cluster of neurons over several weeks, making it useful for long-term behavioral studies. “If you really want to understand what is behind cognition or failures in cognition, like in autism, you need to look at the interaction between neurons,” says lead investigator Edvard Moser, professor of neuroscience at the Kavli Institute for Systems Neuroscience in Trondheim, Norway. Other devices that measure neuronal activity, such as Neuropixels 2.0, record signals from more than 10,000 sites in the brain at once. But they have a low spatial resolution and cannot always determine which specific neuron is firing at any given time. Other miniature microscopes have also, traditionally, relied on visible light, which illuminates the surface of tissue, but are limited to imaging about 2,000 neurons. The new device can monitor a brain area measuring 500 by 500 micrometers and can capture data on more than 10,000 neurons at once. A typical mouse brain is roughly the size of a pea and contains about 85 million neurons. The MINI2P uses infrared light to capture the activity of neurons engineered to express GCaMP, a protein that binds to calcium ions during an action potential and emits a fluorescent signal in reply. The microscope measures that fluorescence using an infrared laser beam. © 2022 Simons Foundation

Keyword: Brain imaging
Link ID: 28282 - Posted: 04.13.2022

Yasemin Saplakoglu Imagine that while you are enjoying your morning bowl of Cheerios, a spider drops from the ceiling and plops into the milk. Years later, you still can’t get near a bowl of cereal without feeling overcome with disgust. Researchers have now directly observed what happens inside a brain learning that kind of emotionally charged response. In a new study published in January in the Proceedings of the National Academy of Sciences, a team at the University of Southern California was able to visualize memories forming in the brains of laboratory fish, imaging them under the microscope as they bloomed in beautiful fluorescent greens. From earlier work, they had expected the brain to encode the memory by slightly tweaking its neural architecture. Instead, the researchers were surprised to find a major overhaul in the connections. What they saw reinforces the view that memory is a complex phenomenon involving a hodgepodge of encoding pathways. But it further suggests that the type of memory may be critical to how the brain chooses to encode it — a conclusion that may hint at why some kinds of deeply conditioned traumatic responses are so persistent, and so hard to unlearn. “It may be that what we’re looking at is the equivalent of a solid-state drive” in the brain, said co-author Scott Fraser, a quantitative biologist at USC. While the brain records some types of memories in a volatile, easily erasable form, fear-ridden memories may be stored more robustly, which could help to explain why years later, some people can recall a memory as if reliving it, he said. Memory has frequently been studied in the cortex, which covers the top of the mammalian brain, and in the hippocampus at the base. But it’s been examined less often in deeper structures such as the amygdala, the brain’s fear regulation center. The amygdala is particularly responsible for associative memories, an important class of emotionally charged memories that link disparate things — like that spider in your cereal. While this type of memory is very common, how it forms is not well understood, partly because it occurs in a relatively inaccessible area of the brain. All Rights Reserved © 2022

Keyword: Learning & Memory; Brain imaging
Link ID: 28241 - Posted: 03.16.2022

by Niko McCarty The ‘opto’ in optogenetics — the powerful method some autism researchers use to control neurons in mice and other animals — comes from the Greek optós, meaning visible. It’s a nod to the blue light used to switch on select neurons. A new technique can do the same, albeit with something invisible: sound. In a study published in Nature Communications this month, researchers engineered neurons in the motor cortex of mice to express an ultrasound-sensitive ion channel protein called hsTRPA1. They placed an ultrasound transducer near the animal’s skull and switched it on. The response? A flex of a muscle, a perceptible twitch. The approach, called sonogenetics, enables noninvasive control over any neural circuit that can be manipulated with optogenetics, an invasive method, says lead investigator Sreekanth Chalasani, associate professor in the Molecular Neurobiology Laboratory at the Salk Institute for Biological Studies in La Jolla, California. Spectrum spoke to Chalasani about his early experiments in Caenorhabditis elegans, lucky number 63 and how sonogenetics could one day have clinical applications. Spectrum: Our readers might be familiar with optogenetics, but I’m assuming sonogenetics is new for most people. Sreekanth Chalasani: Yeah. Well, the idea in sonogenetics is that we want to manipulate things noninvasively. Ultrasound can travel through bone and skin, into the body. We’ve been using it for decades. It’s safe. The question is: Can we leverage it to get in the body and control cells, like with optogenetics? S: Literally controlling cells with sound. SC: Right. In optogenetics, light triggers action potentials in cells that have a channelrhodopsin, or opsin, protein. In sonogenetics, we wanted a protein that would let us have that same level of cellular control. But finding that protein has been difficult. Lots of groups have been looking for these proteins, and we were fortunate to find one. © 2022 Simons Foundation

Keyword: Brain imaging
Link ID: 28227 - Posted: 03.02.2022

By Kim Tingley Denis Burkitt, an Irish surgeon, traveled to Africa during World War II as a member of the Royal Army Medical Corps, and afterward he settled in Uganda to practice medicine. There he observed that a surprising number of children developed strange jaw tumors, a cancer that would come to be known as Burkitt lymphoma. Eventually, Burkitt sent samples of the tumor cells to Middlesex Hospital Medical School in London, where Michael Anthony Epstein, a pathologist, and his colleagues Yvonne Barr and Bert Achong examined them through an electron microscope. Their findings — they noticed particles shaped like a herpesvirus, only smaller — were published in a landmark paper in The Lancet in 1964 and spurred the realization that this newly identified member of the Herpes​viridae family, subsequently named Epstein-Barr virus, was a cause of Burkitt lymphoma. It was the first evidence that a viral infection could lead to cancer. The virus has since been shown to increase the risk of Hodgkin lymphoma, as well as nasopharyngeal and stomach cancer. It is also the virus most often responsible for infectious mononucleosis, a disease usually characterized by extreme fatigue, sore throat, fever and swollen lymph nodes in the neck. These symptoms can last for weeks and, in chronic cases, recur for years. We now know that upward of 90 percent of adults have the Epstein-Barr virus. As happens with other herpes​viruses, once you have been infected, the virus stays with you forever — it deposits its DNA alongside yours in the nucleus of many of your cells. (RNA viruses, like SARS-CoV-2, can be cleared from your body.) Most people contract Epstein-Barr in childhood: It is spread through body fluids, usually saliva; kissing is a frequent route of transmission (as may be the sharing of utensils). Young children, if they get sick at all, typically develop symptoms indistinguishable from those of a cold or flu; mono is more common when the first infection happens after puberty. “Most people never know they’re infected,” says Jeffrey Cohen, the chief of the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases. © 2022 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28223 - Posted: 02.26.2022

Natalia Mesa More than a decade ago, scientists developed optogenetics, a method to turn cells on and off with light. The technique allows scientists to spur or suppress cells' electrical activity with just the flip of a switch to tease apart the roles of specific cell types. But because light doesn’t penetrate deep into tissues, scientists need to surgically implant light sources to illuminate cells below the surface of the skin or skull. In a new study published today (February 9) in Nature Communications, researchers report they’ve found a way to use ultrasound to noninvasively activate mouse neurons, both in culture and in the brains of living animals. The technique, which the authors call sonogenetics, elicits electrical activity in a subset of brain cells that have been genetically engineered to respond to sound waves. “We know that ultrasound is safe,” study coauthor Sreekanth Chalasani, a neuroscientist in Salk’s Molecular Neurobiology Laboratory, tells The Scientist. “The potential for neuronal control is huge. It has applications for pacemakers, insulin pumps, and other therapies that we’re not even thinking about. Jamie Tyler, a biomedical engineer at the University of Alabama at Birmingham who was not involved in the study but has previously collaborated with some of its authors, tells The Scientist that the work represents “more than just a step forward” in being able to use ultrasound to control neural activity: “It shows that sonogenetics is a viable technique in mammalian cells.” © 1986–2022 The Scientist.

Keyword: Brain imaging
Link ID: 28199 - Posted: 02.12.2022