Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 26285

By Sofie Bates In multiple sclerosis, barriers that guard the brain become leaky, allowing some disease-causing immune cells to invade. Now scientists have identified a key molecule in the process that helps B cells breach the barriers. ALCAM, a protein produced by B cells, helps the immune cells sneak into the central nervous system, researchers report November 13 in Science Translational Medicine. Tests in mice and in artificial human brain barriers show that B cells without ALCAM, or activated leukocyte cell adhesion molecule, had trouble getting through the brain’s barriers. And in mice with a disease with some characteristics similar to MS, blocking ALCAM seemed to alleviate the disease’s severity. These early results indicate that the protein may be a good target for new treatments for multiple sclerosis in people, the researchers say. “This is a very important puzzle piece in how we understand multiple sclerosis,” says David Leppert, a neurologist at the University Hospital Basel in Switzerland who was not involved in the work. “How it translates into clinical applications is yet another question.” Worldwide, over 2.3 million people have multiple sclerosis, including nearly 1 million adults in the United States. Scientists think that rogue immune cells invade the brain and strip away the protective coating on nerve cells — leading to neurological issues and physical disability as the disease progresses. There’s no cure, and treatments don’t work for advanced stages of multiple sclerosis. Scientists have developed over a dozen medications to treat MS symptoms (SN: 11/29/17), one of which uses antibodies to destroy the body’s B cells. But that approach weakens patients’ immune systems, opening the door for future infections or cancer. In the new study, the researchers are instead focusing on preventing disease-causing B cells from entering the brain. © Society for Science & the Public 2000–2019

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26859 - Posted: 11.29.2019

Merrit Kennedy A newly published study from University College London suggests that a single dose of ketamine could help dramatically reduce the alcohol intake of heavy drinkers. Bruce Forster/Getty Images What if a single dose of ketamine could make a heavy drinker dramatically cut back on booze? A team at University College London thinks that ketamine may be able to "rewrite" memories that shape a person's relationship with alcohol. Scientists say that participants who were given ketamine as part of an experimental study dramatically reduced their average alcohol intake for months after the initial dose. Their research was published Tuesday in Nature Communications. Ketamine — sometimes known as a club drug called Special K that can produce hallucinations — has been shown to be a powerful and fast-acting treatment for depression. Researchers also are looking into whether ketamine can help patients with post-traumatic stress disorder. The U.K. findings may signal yet another use for the drug for hard-to-treat conditions. In general, the treatment options for alcoholism "aren't particularly effective for the majority of people, particularly over the long term," says Ravi Das, a UCL psychopharmacologist and the study's lead researcher. Das thinks part of the problem is that current remedies don't necessarily help patients deal with positive memories of drinking that could make them want to drink again. "When people become addicted, they're learning that kind of behavior in response to things in their environment," he says. "Those memories, those associative trigger memories, can be really long lasting and really kind of ingrained. And current treatments don't target those." © 2019 npr

Keyword: Drug Abuse
Link ID: 26858 - Posted: 11.29.2019

Suzana Herculano-Houzel Here’s something new to consider being thankful for at the dinner table: the long evolutionary journey that gave you your big brain and your long life. Courtesy of our primate ancestors that invented cooking over a million years ago, you are a member of the one species able to afford so many cortical neurons in its brain. With them come the extended childhood and the pushing century-long lifespan that together make human beings unique. All these bequests of your bigger brain cortex mean you can gather four generations around a meal to exchange banter and gossip, turn information into knowledge and even practice the art of what-not-to-say-when. You may even want to be thankful for another achievement of our neuron-crammed human cortices: all the technology that allows people spread over the globe to come together in person, on screens, or through words whispered directly into your ears long distance. I know I am thankful. But then, I’m the one proposing that we humans revise the way we tell the story of how our species came to be. Back when I had just received my freshly minted Ph.D. in neuroscience and started working in science communication, I found out that 6 in 10 college-educated people believed they only used 10% of their brains. I’m glad to say that they’re wrong: We use all of it, just in different ways at different times. The myth seemed to be supported by statements in serious textbooks and scientific articles that “the human brain is made of 100 billion neurons and 10 times as many supporting glial cells.” I wondered if those numbers were facts or guesses. Did anyone actually know that those were the numbers of cells in the human brain? No, they didn’t. © 2010–2019, The Conversation US, Inc.

Keyword: Intelligence; Neurogenesis
Link ID: 26857 - Posted: 11.29.2019

By Donald McCarthy I lived only half a childhood. Friendships were difficult, because I often did not know what to say. I had little patience for small talk and a dislike of new situations. Thrust into unfamiliar surroundings, my whole body would warm, my hands would shake, and I would feel a tightening in my chest and a deep, almost primal urge to scream. Even as an adult, I felt like I viewed reality through a foggy window. I thought it was simply me — that my personality was just odd — and I would need to learn to cope with the fact that I did not fit in well with most people. Then, at age 28, I was diagnosed with autism spectrum disorder (ASD). My diagnosis was a relief. Suddenly, I knew why I felt the way I did, and why I had a hard time living the way others did. But I can only imagine how much better my life would have been if I had been diagnosed as a child and had the chance to understand myself at a younger age. Might I have made emotional connections with my peers, instead of just with Bruce Springsteen songs and characters in Stephen King novels? It turns out I’m not alone. Many people go more than half of their lives before learning that they are autistic; the exact number remains a mystery, as research on adults with autism has been scarce. Although public awareness of ASD and its symptoms has improved in recent decades, many children still slip through the cracks, especially girls and children of color. We as a society have the power and resources to change that; all we need is the will. Consider the science: There is little question among psychologists specializing in autism that an early diagnosis can change a person’s life for the better. Therapy aimed at reworking the way a young person with ASD thinks and comprehends has shown success. Children who undergo therapy see results that allow them to curb undesirable behavior, improve social interactions, and better their own quality of life.

Keyword: Autism
Link ID: 26856 - Posted: 11.29.2019

Lateshia Beachum A Chinese man sought medical attention for seizures and a headache that lasted nearly a month. Doctors found that tapeworms from undercooked meat were causing his pain. Researchers at the First Affiliated Hospital of Zhejiang University published a paper last week that details the plight of 46-year-old construction worker Zhu (an alias for the patient) in the eastern Zhejiang province of China who bought pork and mutton about a month ago for a spicy hot pot broth. Days later, the man started feeling dizzy, having headaches and experiencing epilepsy-like symptoms such as limb twitching and mouth foaming while trying to sleep at night, according to the report. Co-workers witnessed one of Zhu’s episodes and dialed for emergency help. He was seen at a hospital where scans and tests showed that he had multiple intracranial calcifications, abnormal deposits of calcium in blood vessels to the brain; and multiple intracranial lesions, according to researchers. Medical staff wanted to examine him further, but he dismissed their concerns because he didn’t want to spend more money, according to the report. The symptoms that sent Zhu to the hospital persisted after he left, researchers reported. He became frightened. He spoke with his relatives about seeking medical treatment before deciding on care at the First Affiliated Hospital of Zhejiang University Medical College. Huang Jianrong, the hospital’s chief doctor, consulted Zhu and learned that he had eaten pork and mutton not too long ago, according to the report.

Keyword: Miscellaneous
Link ID: 26855 - Posted: 11.29.2019

By Lisa Sanders, M.D “Where am I?” the 68-year-old man asked. His daughter explained again: He was at Yale-New Haven Hospital in Connecticut. He had been found on the ground in the parking lot of the grocery store near his apartment. The man nodded, as if taking it all in, but minutes later asked again: Where am I? He had never had any memory issues before, but now he couldn’t remember that it was Saturday. Didn’t remember that he spent the morning moving the last of the boxes he had stored at his daughter’s house to his new apartment. He didn’t even remember that he had spent the past few months hashing out a pretty messy divorce. His soon-to-be ex-wife was also in the E.R., and again and again he asked her: Are we really getting divorced? Why? What happened? Earlier that day, his daughter received a call from the hospital saying that her father had fallen outside the supermarket and was brought in by an ambulance called by a good Samaritan. No one could tell her any more than that, and her father clearly didn’t remember. He had a scrape on his right cheek and over his eye, but otherwise he seemed fine. Except he couldn’t remember the events of the recent past. When asked his name and address, he responded promptly, but the address he gave was the house he shared for many years with his future ex-wife. He seemed stunned to find out he no longer lived there. The doctor in the E.R. was also surprised by the extent of the man’s memory loss. He seemed to have lost both his retrograde memory, recall of the events of the recent past, and his anterograde memory, the ability to form new memories from the present. But on examination, everything else seemed basically normal — except that his blood pressure was high, and he had the scrapes on his face. There was no sign of infection. His kidneys and liver seemed to be working just fine. A head CT scan showed no injuries to the bones of the face, the spinal cord in the neck or the brain. There was no trace of alcohol or drugs in his system. After a few hours, the man’s memory was still not functioning properly, and he was admitted to the hospital. © 2019 The New York Times Company

Keyword: Learning & Memory
Link ID: 26854 - Posted: 11.26.2019

Correspondent Lesley Stahl Who among us hasn't wished we could read someone else's mind, know exactly what they're thinking? Well that's impossible, of course, since our thoughts are, more than anything else, our own. Private, personal, unreachable. Or at least that's what we've always, well, thought. Advances in neuroscience have shown that, on a physical level, our thoughts are actually a vast network of neurons firing all across our brains. So if that brain activity could be identified and analyzed, could our thoughts be decoded? Could our minds be read? Well, a team of scientists at Carnegie Mellon University in Pittsburgh has spent more than a decade trying to do just that. We started our reporting on their work 10 years ago, and what they've discovered since, has drawn us back. In Carnegie Mellon's scanner room, two floors underground, a steady stream of research subjects come to have their brains and thoughts "read" in this MRI machine. It's a type of scanning called functional MRI, FMRI. That looks at what's happening inside the brain as a person thinks. Marcel Just: It's like being an astronomer when the first telescope is discovered, or being a biologist when the first microscope is-- is developed. Neuroscientist Marcel Just says this technology has made it possible for the first time to see the physical makeup of our thoughts. When we first visited Dr. Just's lab ten years ago, he and his team had conducted a study. They put people in the scanner and asked them to think about ten objects, five of them tools like screwdriver and hammer and five of them dwellings like igloo and castle, while measuring activity levels throughout their brains. The idea was to crunch the data and try to identify distinctive patterns of activity for each object. Lesley Stahl: You had them think about a screwdriver. Marcel Just: Uh-huh. Lesley Stahl: And the computer found the place in the brain where that person was thinking "screwdriver?" Marcel Just: Screwdriver isn't one place in the brain. It's many places in the brain. When you think of a screwdriver, you think about how you hold it, how you twist it, what it looks like… Lesley Stahl: And each of those functions are in different places? Marcel Just: Correct. He showed us that by dividing the brain into thousands of tiny cubes and analyzing the amount of activity in each one, his team was able to identify unique patterns for each object. © 2019 CBS Interactive Inc.

Keyword: Emotions; Brain imaging
Link ID: 26853 - Posted: 11.26.2019

By Joanne Chen I grew up in New England, so you’d think I’d be used to winter by now. But after wearing dozens of puffy coats thin over my lifetime, that’s not the case: I hate the relentless chill, the heavy boots, the darkness. It’s enough to make anyone want to curl up under a blanket and snooze until March. But as Wirecutter’s sleep writer, I also know that many sleep-promoting products don’t actually do much. Winter tiredness is as mental as it is physical, and you need to consider things both in and out of the bedroom to reawaken your fun-loving self. To help make your seven to eight hours of sleep feel exactly that, here are four expert-approved strategies. Shorter days are largely to blame for the blahs. Light controls our circadian rhythm. Its presence suppresses the flow of the sleep hormone melatonin; its absence encourages it. When sunlight takes its own sweet time to arrive in the morning and slinks away before dinner, that sleepy feeling prevails, even if we’ve just slept. To mimic the refreshing effects of a bright spring morning — but in the darkness of 6 a.m. in winter — a sunrise alarm clock might help. We recommend the Philips Wake-Up Light HF3520. Its light gradually fills the room and peaks at the designated time. There’s a backup alarm too, which I set to the sound of birds chirping so I can pretend it’s actually May. A more integrated strategy: Outfit your home with smart bulbs instead, which you can program to brighten just as you would a sunrise alarm clock. If the thought of entering a dark home after work makes you want to ditch all household obligations, you can also arrange lights to turn on before you walk through your door. Philips Hue, Wirecutter’s smart-bulb pick, offers lighting “formulas” such as brighter intensities in the morning and warmer glows in the evening. (While you’re at it, why not program your smart speaker to play whatever song fires you up?) For an extra kick, light therapy lamps — like our pick, the Carex Day-Light Classic Plus Lamp — might help. Doctors often recommend these for seasonal affective disorder (S.A.D.), a type of depression triggered by certain seasons. (Talk to yours about whether the device is appropriate for you and how best to use it.) © 2019 The New York Times Company

Keyword: Biological Rhythms; Sleep
Link ID: 26852 - Posted: 11.26.2019

By Meredith Wadman Tony Magana, chief of neurosurgery at Mekelle University School of Medicine in Ethiopia’s Tigray province, confronts his country’s high prevalence of neural tube defects nearly every day. His team operates on more than 400 babies annually to repair these severe, often lethal birth malformations, in which babies can be born without brains or with their spinal cords protruding from their backs. “Probably every other day we see a child that is so bad we can’t help them,” Magana says. The holes where the spinal cord protrudes “are so big that you can’t close them.” This month, a team of nutrition experts converged in Addis Ababa to lay groundwork for an unproven but possibly highly effective intervention: fortifying Ethiopia’s salt supply with folic acid, a synthetic form of the B vitamin folate. In the first 4 weeks of pregnancy, folate is essential to proper closure of the neural tube, which gives rise to the brain and spinal cord, and since the mid-1990s, more than 80 countries have mandated flour fortification with folic acid. Ethiopia, where fewer than one-third of people eat flour, is not among them. Last year, a pair of studies that surveyed births at 11 public hospitals there shook the global health community. The studies—one co-authored by Magana—found that among every 10,000 births, between 126 and 131 babies suffered from neural tube defects (NTDs). That’s seven times their global prevalence and 26 times the prevalence in high-income, flour-fortifying countries such as the United States. According to Ethiopian government data, 84% of Ethiopian women of reproductive age have folate levels in their red blood cells that put them at risk of giving birth to a child with an NTD. © 2019 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 26851 - Posted: 11.26.2019

A disturbing aspect of Canada's opioid crisis is that more babies are being born to mothers who use fentanyl and other opioid drugs. The Canadian Institute for Health Information says more than 1,800 infants per year are born with symptoms of opioid withdrawal. A study presented Monday at the 105th Scientific Assembly and Annual Meeting of the Radiological Society of North America suggests that prenatal exposure to opioids may have a significant impact on the brain development of unborn children. A team of obstetricians, neonatologists, psychologists and radiologists led by Dr. Rupa Radhakrishnan, a radiologist at Indiana University School of Medicine, did functional MRI brain scans on 16 full-term infants. Eight of the infants had mothers who used opioids during pregnancy and eight had mothers who did not use opioids. The brain imaging technique used by the researchers is called resting state functional MRI (fMRI). The technique enabled researchers to measure brain activity by detecting changes in blood flow. The technique permits researchers to measure how well different regions of the brain talk to one another. The researchers found abnormal connections to and from a part of the brain called the amygdala. It's a region that is responsible for the perception and regulation of emotions such as anger, fear, sadness and aggression. This is one of the first studies to suggest that the brain function of infants may be affected by prenatal exposure to opioids. Abnormal function in the amygdala could make it difficult for children exposed to opioids to regulate their emotions. That could have serious implications on their social development and on their behaviour. The researchers say the study is small. They say they aren't certain as to the clinical implications of this study. A long-term outcome study is underway to understand better the functional brain changes caused by prenatal opioid exposure and their associated long-term developmental outcomes. How newborns face opioid withdrawal This research may become even more important should current trends continue, and we see an increase in the number of infants exposed to opioids prenatally. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Drug Abuse
Link ID: 26850 - Posted: 11.26.2019

By Nicholas Bakalar Long-term exposure to air pollution is associated with lower scores on tests of mental acuity, researchers have found. And one reason may be that air pollution causes changes in brain structure that resemble those of Alzheimer’s disease. The scientists studied 998 women ages 73 to 87 and free of dementia, periodically giving them tests of learning and memory. They used magnetic resonance imaging to detect brain atrophy, or wasting, and then scored the deterioration on its degree of similarity to the brain atrophy characteristic of Alzheimer’s disease. They matched Environmental Protection Agency data on air pollution to the women’s residential addresses. Over 11 years of follow-up, they found that the greater the women’s exposure to PM 2.5, the tiny particulate matter that easily penetrates the lungs and bloodstream, the lower their scores on the cognitive tests. After excluding cases of dementia and stroke, they also found a possible reason for the declining scores: The M.R.I. results showed that increased exposure to PM 2.5 was associated with increased brain atrophy, even before clinical symptoms of dementia had appeared. The study is in the journal Brain. “PM 2.5 alters brain structure, which then accelerates memory decline,” said the lead author, Diana Younan, a postdoctoral researcher at the University of California. “I just want people to be aware that air pollution can affect their health, and possibly their brains.” © 2019 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 26849 - Posted: 11.26.2019

By James Gorman TEMPE, Ariz. — Xephos is not the author of “Dog Is Love: Why and How Your Dog Loves You,” one of the latest books to plumb the nature of dogs, but she helped inspire it. And as I scratched behind her ears, it was easy to see why. First, she fixed on me with imploring doggy eyes, asking for my attention. Then, every time I stopped scratching she nudged her nose under my hand and flipped it up. I speak a little dog, but the message would have been clear even if I didn’t: Don’t stop. We were in the home office of Clive Wynne, a psychologist at Arizona State University who specializes in dog behavior. He belongs to Xephos, a mixed breed that the Wynne family found in a shelter in 2012. Dr. Wynne’s book is an extended argument about what makes dogs special — not how smart they are, but how friendly they are. Xephos’ shameless and undiscriminating affection affected both his heart and his thinking. As Xephos nose-nudged me again, Dr. Wynne was describing genetic changes that occurred at some point in dog evolution that he says explain why dogs are so sociable with members of other species. “Hey,” Dr. Wynne said to her as she tilted her head to get the maximum payoff from my efforts, “how long have you had these genes?” No one disputes the sociability of dogs. But Dr. Wynne doesn’t agree with the scientific point of view that dogs have a unique ability to understand and communicate with humans. He thinks they have a unique capacity for interspecies love, a word that he has decided to use, throwing aside decades of immersion in scientific jargon. © 2019 The New York Times Company

Keyword: Sexual Behavior; Language
Link ID: 26848 - Posted: 11.23.2019

By Tina Hesman Saey Picking embryos based on genetics might not give prospective parents the “designer baby” they’re after. DNA predictions of height or IQ might help would-be parents select an embryo that would grow into a child who is, at most, only about three centimeters taller or about three IQ points smarter than an average embryo from the couple, researchers report November 21 in Cell. But offspring predicted by their DNA to be the tallest among siblings were actually the tallest in only seven of 28 real families, the study found. And in five of those families, the child predicted to be tallest was actually shorter than the average for the family. Even if it were ethical to select embryos based on genetic propensity for height or intelligence, “the impact of doing so is likely to be modest — so modest that it’s not likely to be practically worth it,” says Amit Khera, a physician and geneticist at the Center for Genomics Medicine at Massachusetts General Hospital in Boston who was not involved in the new study. For years, couples have been able to use genetic diagnosis to screen out embryos carrying a disease-causing DNA variant. The procedure, called preimplantation genetic diagnosis, or PGD, involves creating embryos through in vitro fertilization. Clinic staff remove a single cell from the embryo and test its DNA for genetic variants that cause cystic fibrosis, Tay-Sachs or other life-threatening diseases caused by defects in single genes. © Society for Science & the Public 2000–2019

Keyword: Genes & Behavior; Intelligence
Link ID: 26847 - Posted: 11.23.2019

By Julie Creswell and Sheila Kaplan SAN FRANCISCO — In the face of mounting investigations, subpoenas and lawsuits, Juul Labs has insisted that it never marketed or knowingly sold its trendy e-cigarettes and flavored nicotine pods to teenagers. As youth vaping soared and “juuling” became a high school craze, the company’s top executives have stood firm in their assertion that Juul’s mission has always been to give adult smokers a safer alternative to cigarettes, which play a role in the deaths of 480,000 people in the United States each year. “We never wanted any non-nicotine user and certainly nobody underage to ever use Juul products,” James Monsees, a co-founder of the company, testified at a congressional hearing in July. But in reality, the company was never just about helping adult smokers, according to interviews with former executives, employees and investors, along with reviews of legal filings and social media archives. Juul’s remarkable rise to resurrect and dominate the e-cigarette business came after it began targeting consumers in their 20s and early 30s, a generation with historically low smoking rates, in a furious effort to reward investors and capture market share before the government tightened regulations on vaping. As recently as 2017, as evidence grew that high school students were flocking to its sleek devices and flavored nicotine pods, the company refused to sign a pledge not to market to teenagers as part of a lawsuit settlement. It wasn’t until the summer of 2018, when the Food and Drug Administration required it to do so, that the company put a nicotine warning label on its packaging. Though some former employees recalled Mr. Monsees wearing a T-shirt at the office that used an expletive to refer to Big Tobacco, the start-up’s early pitches to potential investors listed selling the business to a big tobacco company as one of the potential ways to cash out. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26846 - Posted: 11.23.2019

By Veronique Greenwood A few years back, Ryan Herbison, then a graduate student in parasitology at the University of Otago, painstakingly collected about 1,300 earwigs and more than 2,500 sandhoppers from gardens and a beach in New Zealand. Then, he dissected and examined the insides of their heads. This macabre scavenger hunt was in search of worms that lay coiled within some of the insects. The worms are parasites that force earwigs and sandhoppers to march into bodies of water, drowning themselves so the worms’ aquatic offspring can thrive. “Like a back-seat driver, but a bit more sinister,” said Mr. Herbison, describing these mind-controlling parasites. “And sometimes they may just grab the steering wheel.” Just how they do that, though, has remained a bit of a mystery. But in a paper published Wednesday in Proceedings of the Royal Society B, Mr. Herbison and fellow researchers reported that the parasites seemed to be manipulating the production of host proteins involved in generating energy and movement in their unfortunate hosts. The analysis is limited, but the researchers speculated that the parasites may be affecting neuronal connections in the bugs’ brains and perhaps even interfering with memory in a way that puts the hosts at risk. Parasites use a variety of similar strategies. Some make cat urine suicidally attractive to mice, which are promptly eaten so that the parasites can go through the next phase of their life cycle in the cat. Others prompt ants to expose themselves on high tree branches, the better to be eaten by birds. And still others cause snails to hang out in open spaces, with swollen eyestalks pulsing like neon signs, for apparently the same reason. © 2019 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 26845 - Posted: 11.22.2019

Cody A. Siciliano Some individuals consume alcohol their entire adult life without developing an alcohol use disorder. Others, however, quickly transition to compulsive and problematic drinking. Can we determine what makes some people vulnerable to addiction? Alcohol drinking is the third leading cause of preventable death in the United States, and is responsible for millions of deaths per year worldwide. If the reasons why some people are susceptible to alcohol use disorder were known, it might be possible to more effectively treat this devastating disease, or even intervene before serious problems emerge. I have spent my career as a neuroscientist and pharmacologist trying to understand how drugs and alcohol act on the brain, and what makes a brain more or less susceptible to substance use disorders. My laboratory at the Vanderbilt Center for Addiction Research develops approaches for studying addictive behaviors in rats and mice. Using electrochemical and optical approaches to measure brain activity, our goal is to determine how patterns of activity in brain cells give rise to these behaviors – and how we may use this information to treat or prevent substance use disorders. In a report published in the Nov. 22 issue of the journal Science, Kay Tye of the Salk Institute and I set out to understand how binge drinking alters the brain and how this can lead to compulsive behaviors in some drinkers. To study this, we designed an experiment in which mice were scored for their propensity to drink alcohol. We measured compulsive drinking by determining how much they drank when we mixed the alcohol with a bitter tasting substance that mice normally avoid. © 2010–2019, The Conversation US, Inc.

Keyword: Drug Abuse; Brain imaging
Link ID: 26844 - Posted: 11.22.2019

Ruth Williams After copulation, Drosophila melanogaster females are able to create long-term memories of unpleasant events—electric shocks—that virgin females cannot, according to a study published today in Science Advances (November 20). The authors suspect the memory boost may improve the chance of survival of the female during the subsequent egg-laying period as well as guide her choice of laying sites. Whatever the reason, the enhanced memory joins a list of physiological and behavioral effects on female flies that result from sex. “It’s quite impressive and convincing [data],” says entomologist Elwyn Isaac of the University of Leeds who was not involved in the research. “They propose that the sex peptide gets into the [female’s] circulation and somehow gets across the blood brain barrier [to activate memory].” It’s “very interesting,” Isaac continues, because until now, sex peptide—a protein produced in the male reproductive system and found in ejaculate—was thought to act on sensory neurons in the female’s uterus. These neurons produce a receptor protein to which sex peptide binds and are thought to be necessary for the peptide’s many effects on females, which include ramping up ovulation, increasing egg-laying behavior, changing food preference to a high-protein diet, and causing the female to reject other males. But, the authors of the new study, “show definitely that those neurons are not required for this [long-term memory] effect,” Isaac says. Indeed, deletion of the receptor in these neurons made no difference to the flies’ long-term memory formation after sex. © 1986–2019 The Scientist

Keyword: Learning & Memory; Sexual Behavior
Link ID: 26843 - Posted: 11.22.2019

By John Williams Credit...Sonny Figueroa/The New York Times Let’s get right to the overwhelming question: What does it mean to experience something? Chances are that when you recount a great meal to a friend, you don’t say that it really lit up your nucleus of the solitary tract. But chances are equally good, if you adhere to conventional scientific and philosophical wisdom, that you believe the electrical activity in that part of your brain is what actually accounts for the sensation when you dine. In “Out of My Head,” the prolific British writer Tim Parks adds to the very long shelf of books about what he calls the “deep puzzle of minute-by-minute perception.” The vast majority of us — and this is undoubtedly for the best, life being hard enough — don’t get tripped up by the ontological mysteries of our minute-to-minute perceiving. We just perceive. But partly because it remains a stubborn philosophical problem, rather than a neatly explained scientific one, consciousness — our awareness, our self-awareness, our self — makes for an endlessly fascinating subject. And Parks, though not a scientist or professional philosopher, proves to be a companionable guide, even if his book is more an appetizer than a main course. He wants “simply” to ask, he writes, whether “we ordinary folks” can say anything useful about consciousness. But he also wants to poke skeptically at the “now standard view of conscious experience as something locked away in the head,” the “dominant internalist model which assumes the brain is some kind of supercomputer.” “Out of My Head” was inspired, in large part, by the theories of Riccardo Manzotti, a philosopher, roboticist and friend of Parks with whom the author has had “one of the most intense and extended conversations of my life.” (A good chunk of that conversation appeared as a 15-part dialogue on the website of The New York Review of Books, whose publishing arm has released “Out of My Head.”) © 2019 The New York Times Company

Keyword: Consciousness
Link ID: 26842 - Posted: 11.22.2019

Jon Hamilton When we hear a sentence, or a line of poetry, our brains automatically transform the stream of sound into a sequence of syllables. But scientists haven't been sure exactly how the brain does this. Now, researchers from the University of California, San Francisco, think they've figured it out. The key is detecting a rapid increase in volume that occurs at the beginning of a vowel sound, they report Wednesday in Science Advances. "Our brain is basically listening for these time points and responding whenever they occur," says Yulia Oganian, a postdoctoral scholar at UCSF. The finding challenges a popular idea that the brain monitors speech volume continuously to detect syllables. Instead, it suggests that the brain periodically "samples" spoken language looking for specific changes in volume. The finding is "in line" with a computer model designed to simulate the way a human brain decodes speech, says Oded Ghitza, a research professor in the biomedical engineering department at Boston University who was not involved in the study. Detecting each rapid increase in volume associated with a syllable gives the brain, or a computer, an efficient way to deal with the "stream" of sound that is human speech, Ghitza says. And syllables, he adds, are "the basic Lego blocks of language." Oganian's study focused on a part of the brain called the superior temporal gyrus. "It's an area that has been known for about 150 years to be really important for speech comprehension," Oganian says. "So we knew if you can find syllables somewhere, it should be there." The team studied a dozen patients preparing for brain surgery to treat severe epilepsy. As part of the preparation, surgeons had placed electrodes over the area of the brain involved in speech. © 2019 npr

Keyword: Language; Hearing
Link ID: 26841 - Posted: 11.21.2019

Alejandra Manjarrez Typically, the worm Caenorhabditis elegans falls asleep after it experiences stress or hours of swimming. In a recent study, scientists observed another sleep trigger: being confined to a microfluidic chamber. As such devices are widely used to analyze different worm behaviors, the authors caution that the sleep induction could interfere with data interpretation. The results were published November 6 in Nature Communications. “In our field, microfluidic chambers have become very commonly used, and they are valuable tools for precise environmental control and for neural imaging . . . but what this study highlights is that we are significantly impacting the physiology and behavior of these animals by confining them in such a way,” says Cheryl Van Buskirk, a geneticist at California State University in Northridge. Van Buskirk studies sleep and stress response in worms, but she was not involved in this research. The team first observed this behavior while developing a technique to make electrical measurements of individual cells in worms placed in microfluidic chambers. They noticed that the muscle cells of these animals would not show any activity during some periods of time. Inactivity, however, is not always equivalent to sleep. “There are specific criteria for sleep, so we actually spent a good deal of the [latest] paper testing those specific criteria,” says Daniel Gonzales, who participated in this study as a graduate student at Rice University in Houston, but has now moved to Purdue University in Indiana. They tested, for example, whether this behavior was reversible, if it was associated with a decreased response to stimuli, and if the worms took on a stereotypical sleep posture. They found that, in addition to fulfilling these criteria, this microfluidics-induced quiescence was also regulated by neurons previously reported to control sleep in C. elegans. © 1986–2019 The Scientist.

Keyword: Sleep
Link ID: 26840 - Posted: 11.21.2019