Chapter 5. Hormones and the Brain

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Sophie Fessl The hormone irisin is necessary for the cognitive benefits of exercise in healthy mice and can rescue cognitive decline associated with Alzheimer’s disease, according to a study published August 20 in Nature Metabolism. According to the authors, these results support the hypothesis that irisin undergirds the cognitive benefits of exercise—a link that has been long debated. In addition, this study has “paved the way for thinking whether irisin could be a therapeutic agent against Alzheimer’s disease,” says biologist Steffen Maak with the Leibniz Institute for Farm Animal Biology in Germany, who has been critical of the methods used to study irisin in the past and was not involved in the study. Many studies have found that exercise is good for the brain, but the molecular mechanisms responsible for the cognitive boost have remained elusive. During her postdoctoral studies, neuroscientist Christiane Wrann found that the gene that codes for irisin becomes highly expressed in the brain during exercise—one of the first studies linking irisin with the brain. See “Irisin Skepticism Goes Way Back” When she joined the faculties at Massachusetts General Hospital and Harvard Medical School, she decided to investigate the hormone further. Wrann, who holds a patent related to irisin and is academic cofounder and consultant for Aevum Therapeutics, a company developing drugs that harness the protective molecular mechanisms of exercise to treat neurodegenerative and neuromuscular disorders, began to investigate whether irisin mediates the positive effects of exercise on the brain. © 1986–2021 The Scientist.

Keyword: Learning & Memory; Hormones & Behavior
Link ID: 27985 - Posted: 09.13.2021

By Lisa Sanders, M.D. The young woman was awakened by the screams of her 39-year-old husband. “Please make it stop!” he shouted, leaping from the bed. “It hurts!” He paced back and forth across the room, arms crossed over his chest as if to protect himself. Two days earlier, he had inhaled a breath mint when his wife startled him. He felt it move slowly down his throat as he swallowed repeatedly. His chest had hurt ever since. But not like this. The man squirmed miserably throughout the short drive to the emergency room at Westerly Hospital, near the Rhode Island and Connecticut border. No position was comfortable. Everything hurt. Even breathing was hard. Although the doctors in the E.R. immediately determined that the young man wasn’t having a heart attack, it was clear something was very wrong. His blood pressure was so low that it was hard to measure. A normal blood pressure may be 120/80. On arrival, his was 63/32. With a pressure this low, blood couldn’t get everywhere it was needed — a condition known as shock. His lips, hands and feet had a dusky hue from this lack of well-​oxygenated blood. He was given intravenous fluids to bring up his pressure, and when that didn’t work, he was started on medications for it. Three hours later, he was on two of these medicines and his fourth liter of fluid. Despite that, his pressure remained in the 70s. He had to be put on a breathing machine to help him keep up with his body’s demand for more oxygen. The most common cause of shock is infection. But this man, as sick as he was, had no signs of infection. The medical team started him on antibiotics anyway. Could the painful mint have torn his esophagus? Up to 50 percent of patients with that injury will die. A CT scan showed no evidence of perforation or of fluid in his chest. What else could this be? There was no sign of a clot keeping blood from entering the lungs, another cause of deadly low blood pressure. An ultrasound of the heart showed that he had some fluid in the sac called the pericardium, which contains and protects the heart, but not enough to interfere with how well it was beating. He was tested for Covid and for recreational drugs — both negative. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Neuroimmunology
Link ID: 27981 - Posted: 09.08.2021

by Angie Voyles Askham Male mice exposed to atypically low levels of a placental hormone in the womb have altered brain development and asocial behaviors, according to a new study. The findings may help explain why preterm birth — which coincides with a deficiency in hormones made by the placenta — is linked to an increased likelihood of having autism. The hormone, called allopregnanolone, crosses the blood-brain barrier, binds to receptors for the chemical messenger gamma-aminobutyric acid (GABA) and helps regulate aspects of neurodevelopment, including the growth of new neurons. Its levels typically peak in the fetus during the second half of gestation. In the new study, researchers engineered a mouse model to have low fetal levels of allopregnanolone, mimicking the hormone’s loss due to preterm birth or placental dysfunction. The male mice in particular have structural changes in the cerebellum, a brain region known for balance and motor control, and exhibit more pronounced autism-like traits than control mice or female model mice. The new model “has a good translational potential for understanding the underlying mechanisms of sex differences in neurodevelopmental conditions such as autism,” says Amanda Kentner, professor of psychology at the Massachusetts College of Pharmacy and Health Sciences in Boston, who was not involved in the work. Injecting a pregnant mouse with allopregnanolone partway through gestation decreased the likelihood that its offspring would have autism-like traits, the researchers found. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27977 - Posted: 09.04.2021

By Gretchen Reynolds An intriguing new study shows how exercise may bolster brain health. The study was in mice, but it found that a hormone produced by muscles during exercise can cross into the brain and enhance the health and function of neurons, improving thinking and memory in both healthy animals and those with a rodent version of Alzheimer’s disease. Earlier research shows that people produce the same hormone during exercise, and together the findings suggest that moving could alter the trajectory of memory loss in aging and dementia. We have plenty of evidence already that exercise is good for the brain. Studies in both people and animals show that exercise prompts the creation of new neurons in the brain’s memory center and then helps those new cells survive, mature and integrate into the brain’s neural network, where they can aid in thinking and remembering. Large-scale epidemiological studies also indicate that active people tend to be far less likely to develop Alzheimer’s disease and other forms of dementia than people who rarely exercise. But how does working out affect the inner workings of our brains at a molecular level? Scientists have speculated that exercise might directly change the biochemical environment inside the brain, without involving muscles. Alternatively, the muscles and other tissues might release substances during physical activity that travel to the brain and jump-start processes there, leading to the subsequent improvements in brain health. But in that case, the substances would have to be able to pass through the protective and mostly impermeable blood-brain barrier that separates our brains from the rest of our bodies. Those tangled issues were of particular interest a decade ago to a large group of scientists at Harvard Medical School and other institutions. In 2012, some of these researchers, led by Bruce M. Spiegelman, the Stanley J. Korsmeyer Professor of Cell Biology and Medicine at the Dana-Farber Cancer Institute and Harvard Medical School, identified a previously unknown hormone produced in the muscles of lab rodents and people during exercise and then released into the bloodstream. They named the new hormone irisin, after the messenger god Iris in Greek mythology. © 2021 The New York Times Company

Keyword: Learning & Memory; Muscles
Link ID: 27961 - Posted: 08.25.2021

By Kim Tingley During menopause, which marks the end of a woman’s menstrual cycles, her ovaries stop producing the hormones estrogen and progesterone, bringing an end to her natural childbearing years. But those hormones also regulate how the brain functions, and the brain governs their release — meaning that menopause is a neurological process as well. “Many of the symptoms of menopause cannot possibly be directly produced by the ovaries, if you think about the hot flashes, the night sweats, the anxiety, the depression, the insomnia, the brain fog,” says Lisa Mosconi, an associate professor of neurology at Weill Cornell Medicine and director of its Women’s Brain Initiative. “Those are brain symptoms, and we should look at the brain as something that is impacted by menopause at least as much as your ovaries are.” In June, Mosconi and her colleagues published in the journal Scientific Reports one of the few studies to observe in detail what happens to the brain throughout the menopause transition, not just before and after. Using various neuroimaging techniques, they scanned the brains of more than 160 women between the ages of 40 and 65 who were in different stages of the transition to examine the organ’s structure, blood flow, metabolism and function; they did many of the same scans two years later. They also imaged the brains of men in the same age range. “What we found in women and not in men is that the brain changes quite a lot,” Mosconi says. “The transition of menopause really leads to a whole remodeling.” On average, women in the United States enter the menopause transition — defined as the first 12 consecutive months without a period — at around 50; once diagnosed, they are in postmenopause. But they may begin to have hormonal fluctuations in their 40s. (For some women, this happens in their 30s, and surgical removal of the ovaries causes immediate menopause, as do some cancer treatments.) Those fluctuations cause irregular periods and potentially a wide variety of symptoms, including hot flashes, insomnia, mood swings, trouble concentrating and changes in sexual arousal. During this phase, known as perimenopause, which averages four years in length (but can last from several months to a decade), Mosconi and colleagues observed that their female subjects experienced a loss of both gray matter (the brain cells that process information) and white matter (the fibers that connect those cells). Postmenopause, however, that loss stopped, and in some cases brain volume increased, though not to its premenopausal size. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27917 - Posted: 07.21.2021

By Gina Kolata Obesity has stalked Marleen Greenleaf, 58, all of her life. Like most people with obesity, she tried diet after diet. But the weight always came back. With that, she has suffered a lifetime of scorn and stigma. Jeering comments from strangers when she walked down the street. Family members who told her, when she trained for a half-marathon, “I don’t think it’s good for you.” Then, in 2018, Ms. Greenleaf, an administrator at a charter school in Washington, D.C., participated in a clinical trial for semaglutide, which is a new type of obesity drug, known as incretins. Over the course of the 68-week study, Ms. Greenleaf slowly lost 40 pounds. Until then, she had always believed that she could control her weight if she really tried. “I thought I just needed more motivation,” she said. But when she took semaglutide, she said that “immediately, the urge to eat just dissipated.” Incretins appear to elicit significant weight loss in most patients, enough to make a real medical and aesthetic difference. But experts hope that the drugs also do something else: change how society feels about people with obesity, and how people with obesity feel about themselves. If these new drugs allow obesity to be treated like a chronic disease — with medications that must be taken for a lifetime — the thought is that doctors, patients and the public might understand that obesity is truly a medical condition. © 2021 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 27821 - Posted: 05.15.2021

Rebecca Brooker & Tristin Nyman Even before the pandemic, there was plenty for expectant mothers to worry about. Pregnant women must withstand a barrage of arguably well-intentioned, but often hyperbolic, warnings about their health and what’s to come, including concerns about everything from what to eat, to what to wear, to how to feel. Health professionals know that mothers-to-be experience predictable increases in anxiety levels before infants are born. Maternal mental health has been steadily deteriorating in the U.S., particularly among poor and minority women. The calls to “be afraid, be very afraid” are, of course, countered by the equally strong cautions for pregnant women to not worry too much, lest it lead to long-term negative outcomes for them and their infants. Such warnings are not entirely off base. Maternal stress hormones cross the placenta and affect the vulnerable fetus. Fetal exposure to the stress hormone cortisol has been linked to an array of negative outcomes, including miscarriage and preterm birth, and irritable temperament for the child and increased risk of emotional problems during childhood. One thing researchers know is that anxious mothers tend to have anxious children. This common, albeit not prescriptive, phenomenon is likely due to numerous factors, both pre- and postpartum. In our laboratory, we focus on what happens when women start their pregnancies already worried or anxious and what clues we can uncover about how to help them and their children. Our research suggests that worry during pregnancy can have long-term impacts on how mothers’ brains communicate – but also that there might be some simple steps that can help rein in the effects. © 2010–2021, The Conversation US, Inc.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27820 - Posted: 05.15.2021

By Lisa Sanders, M.D. “I can’t move my legs,” the 26-year-old man told his younger brother, who towered above him as he lay sprawled on the floor. He’d been on his computer for hours, he explained, and when he tried to stand up, he couldn’t. His legs looked normal, felt normal, yet they wouldn’t move. At first, he figured his legs must have fallen asleep. He pulled himself up, leaning on his desk, and slowly straightened until he was standing. He could feel the weight on his feet and knees. He let go of the desk and commanded his legs to move. Instead, they buckled, and he landed on the floor with a thud. His brother awkwardly pulled him onto the bed. Then they waited. Surely this weird paralysis would disappear just as suddenly as it came. An hour passed, then two. I’m calling an ambulance, the younger brother announced finally. Reluctantly, the elder agreed. He was embarrassed to be this helpless but worried enough to want help. When the E.M.T.s arrived, they were as confused as the brothers. The medics asked what the young man had been up to. Nothing bad, he assured them. For the past few weeks he had been getting back into shape. He changed his diet, cut out the junk and was drinking a protein concoction that was supposed to help him build muscle. And he was working out hard every day. He’d lost more than 20 pounds, he added proudly. © 2021 The New York Times Company

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27813 - Posted: 05.12.2021

By Lisa Sanders, M.D. It was dark by the time the 41-year-old woman was able to start the long drive from her father’s apartment in Washington, D.C., to her home in Westchester County, N.Y. She was eager to get back to her husband and three children. Somewhere after she crossed the border into Maryland, the woman suddenly developed a terrible itch all over her body. She’d been a little itchy for the past couple of weeks but attributed that to dry skin from her now-faded summertime tan. This seemed very different: much stronger, much deeper. And absolutely everywhere, all at the same time. The sensation was so intense it was hard for the woman to pay attention to the road. She found herself driving with one hand on the steering wheel and the other working to respond to her skin’s new need. There was no rash — or at least nothing she could feel — just the terrible itch, so deep inside her skin that she felt as if she couldn’t scratch hard enough to really get to it. By the light of the Baltimore Harbor Tunnel she saw that her nails and fingers were dark with blood. That scared her, and she tried to stop scratching, but she couldn’t. It felt as if a million ants were crawling all over her body. Not on her skin, but somehow under it. The woman had gone to Washington to help her elderly father move. His place was a mess. Many of his belongings hadn’t been touched in years. She figured that she was having a reaction to all the dust and dirt and who knows what else she encountered while cleaning. As soon as she got home, she took a long shower; the cool water soothed her excoriated skin. She lathered herself with moisturizer and sank gratefully into her bed. But the reprieve didn’t last, and from that night on she was tormented by an itch that no scratching could satisfy. © 2021 The New York Times Company

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 27775 - Posted: 04.17.2021

by Peter Hess Mice missing a copy of the autism-linked gene MAGEL2 have trouble discerning between a familiar mouse and an unfamiliar one, but treating them with the social hormone vasopressin reverses this deficit, according to a new study. Mutations in or deletions of MAGEL2 are linked to autism and several related conditions, including Prader-Willi syndrome, which is characterized by intellectual disability, poor muscle tone, difficulty feeding and problems with social interactions. The new findings suggest that these social issues in people stem from impairments in vasopressin’s function in a brain region called the lateral septum, which relays signals between the hippocampus and the ventral tegmental area. They also hint that vasopressin treatment could remedy those issues, says Elizabeth Hammock, assistant professor of psychology and neuroscience at Florida State University in Tallahassee, who was not involved with the study. A 2020 study showed that low levels of vasopressin in cerebrospinal fluid can flag many infants who are later diagnosed with autism. But clinical trials have shown that either providing vasopressin or blocking its effects can improve social communication in autistic children. Because of these seemingly contradictory results, “a better understanding of how alterations in the vasopressinergic system leads to social deficits and how vasopressin administration could resolve some of these problems was needed,” says co-lead researcher Freddy Jeanneteau, professor of neuroscience at Montpellier University in Montpellier, France. © 2021 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27665 - Posted: 01.27.2021

by Peter Hess Two types of neurons process social information, a new mouse study suggests, but only one is disrupted in mice missing the autism-linked gene FMR1. The neurons reside in a brain region called the hypothalamus, and both send signals via the hormone oxytocin. The deletion of FMR1, however, affects these cells differently: The loss of FMR1 in the smaller, ‘parvocellular’ neurons diminishes the mice’s interest in social interactions — but only those involving peers, the new work shows. The gene’s loss from the larger, ‘magnocellular’ neurons, by contrast, does not disrupt the animals’ interactions with either peers or parents. “There are a lot of different types of social behaviors, and not all of them are impaired in autism,” says lead investigator Gül Dölen, assistant professor of neuroscience at Johns Hopkins University in Baltimore, Maryland. Whereas peer-to-peer social interactions are troublesome for many autistic people, other social interactions — such as parental connections — are on par with those seen in non-autistic people, she says. This new understanding of the different neurons’ functions could help explain why clinical trials of oxytocin for treating autism traits have shown mixed results. It could also help scientists develop more effective treatments, experts say. “There are these two different kinds of neurons that we’ve known about for a really long time, and each of their contributions to social behavior has never really been dissected out,” says Larry Young, chief of behavioral neuroscience and psychiatric disorders at Emory University in Atlanta, Georgia, who was not involved with the study. “It’s really important for the future of drug development.” © 2020 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27632 - Posted: 12.19.2020

By Sally Satel For over a half-century, steroid drugs have been a mainstay of medical care, widely used to treat inflammatory illness such as asthma, skin conditions and autoimmune diseases. Less is known about their dramatic and sometimes frightening long-term effects on mood, personality and thinking. I took steroids years ago, and the side effects changed my life. Steroid medications mimic a natural hormone in the body called glucocorticoid, which suppresses immune system processes that trigger inflammation, the sources of many autoimmune and chronic disease. In 1948, glucocorticoid was first used for a chronic inflammatory disease, rheumatoid arthritis, which causes joint deformity and chronic pain. Two years later, the American physician behind the breakthrough therapy was one of the winners of the Nobel Prize. Steroids have been prescribed for many other conditions since then. One steroid, dexamethasone, has been used for people with severe cases of covid-19 and President Trump was given it when he was hospitalized for the disease in October. My story starts in 1977. I was finishing my senior year as a biology major at Cornell University when I was diagnosed with Crohn’s disease, a form of inflammatory disease in which the body’s immune system attacks the gastrointestinal tract. I had a relatively mild case — transient pain, causing me to rush to the nearest ladies’ room, and find some blood in the bowl — and so I was able to finish my final year on time and begin a PhD program in evolutionary biology that summer. My predoctoral project entailed measuring the jaw muscles of tadpoles using jewelers’ tools and a dissecting microscope. Within weeks, though, I had a “flare” in the parlance of gastroenterology — I felt weak and was having increased bouts of blood-streaked diarrhea. In mid-October, I spent five days at the hospital where my symptoms resolved on a daily regimen of 60 mg of the potent steroid prednisone. I was discharged on 60 mg per day and felt fine for a week. But soon my brain began to feel like cotton wrapped in yards of gauze. I tried to study for an upcoming quiz but I couldn’t concentrate. © 1996-2020 The Washington Post

Keyword: Hormones & Behavior
Link ID: 27609 - Posted: 12.07.2020

Moles have a pretty tough life. They live underground, in the dark, burrowing through heavy dirt. And when faced with an enemy, there's nowhere to turn — they have to fight. In most mammals, females tend to be at a disadvantage when it comes to face-to-face combat, because they tend to be smaller and less aggressive than males. But female moles have evolved a secret weapon: a hybrid organ made up of both ovarian and testicular tissue. This effectively makes them intersex, giving them an extra dose of testosterone to make them just as muscular and aggressive as male moles. "As a consequence, basically the whole body of the female, they get masculinized," geneticist Darío Lupiáñez told Quirks & Quarks host Bob McDonald. "They become the body builders of nature." Lupiáñez co-led a study to understand how the moles' genes facilitated this advantage, which was recently published in the journal Science. The research was part of a collaboration between the Max Planck Institute for Molecular Genetics and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Germany. Same genes, different instructions The team worked with Iberian moles, commonly found in Spain and Portugal, however this intersex adaptation has been documented in at least six mole species. "We know that intersexuality happens in species like humans, dogs or cats. But the difference actually in moles, it happens all the time, so all the females are intersexual. And this is really something unique among mammals," said Lupiáñez. To understand how moles evolved these intersexual traits, researchers fully mapped the genome of the Iberian mole, commonly found in Spain and Portugal. (David Carmona, Department of Genetics, University of Granada, Spain ) ©2020 CBC/Radio-Canada.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27530 - Posted: 10.19.2020

By Lisa Sanders, M.D. The waiter had barely put the plate in front of her when the 46-year-old woman felt the color drain from her face. She was in Fresno, Calif., on a work trip and had come to a restaurant to meet an old friend for dinner. But all of a sudden her stomach dropped — the way it might on a roller-coaster ride. A sudden coolness on her face told her she’d broken out in a sweat. She felt dizzy and a little confused. She saw the alarmed face of her friend and knew she looked as bad as she felt. She excused herself and carefully made her way to the bathroom. She sat in front of the vanity and supported her head on her arms. There was the now-familiar stabbing pain in her stomach. She wasn’t sure how long she stayed like that. Was it 10 minutes? 15? At last she felt as if she could get up. As she hurried to meet her friend at the entrance, she felt the contents of her stomach surging upward. She covered her mouth as vomit shot between her fingers. She lowered her head and bolted through the doorway, trying not to see the horrified faces of the diners. In the parking lot, the rush of stomach contents continued until she was completely empty. Exhausted, she sank into the seat of her friend’s car. She was too sick to go back to her hotel, her friend said. Instead the friend would take her to her house, until she felt better. The next thing the woman remembered was that she was sitting on the floor of her friend’s shower, hot water pounding her back. When she could, she crawled into bed. She slept until late the next morning. She thanked her friend, canceled her morning meetings and later that day headed home to Stockton, Calif. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27498 - Posted: 09.30.2020

David Cox Gérard Karsenty was a young scientist trying to make a name for himself in the early 1990s when he first stumbled upon a finding that would go on to transform our understanding of bone, and the role it plays in our body. Karsenty had become interested in osteocalcin, one of the most abundant proteins in bone. He suspected that it played a crucial role in bone remodelling – the process by which our bones continuously remove and create new tissue – which enables us to grow during childhood and adolescence, and also recover from injuries. Intending to study this, he conducted a genetic knockout experiment, removing the gene responsible for osteocalcin from mice. However to his dismay, his mutant mice did not appear to have any obvious bone defects at all. “For him, it was initially a total failure,” says Mathieu Ferron, a former colleague of Karsenty who now heads a research lab studying bone biology at IRCM in Montreal. “In those days it was super-expensive to do modification in the mouse genome.” But then Karsenty noticed something unexpected. While their bones had developed normally, the mice appeared to be both noticeably fat and cognitively impaired. “Mice that don’t have osteocalcin have increased circulating glucose, and they tend to look a bit stupid,” says Ferron. “It may sound silly to say this, but they don’t learn very well, they appear kind of depressed. But it took Karsenty and his team some time to understand how a protein in bone could be affecting these functions. They were initially a bit surprised and terrified as it didn’t really make any sense to them.” © 2020 Read It Later, Inc.

Keyword: Hormones & Behavior; Obesity
Link ID: 27473 - Posted: 09.16.2020

Sean Ingle The double Olympic 800m champion Caster Semenya appears to have lost her long-running legal battle against regulations requiring women with high testosterone to take medication to compete internationally between 400m and a mile. A Swiss federal tribunal said on Tuesday that it supported a decision by the court of arbitration for sport last year that track and field’s policy for athletes with differences in sex development (DSD) was “necessary, reasonable and proportionate” to ensure fair competition in women’s sport. Charley Hull withdraws from ANA Inspiration after positive Covid-19 test Read more “Based on these findings, the Cas decision cannot be challenged,” the tribunal said. “Fairness in sport is a legitimate concern and forms a central principle of sporting competition. It is one of the pillars on which competition is based.” It now looks impossible for Semenya, the London 2012 and Rio 2016 gold medallist, to defend her title in Tokyo. She responded to the news by accusing World Athletics of being on the “wrong side of history”. “I am very disappointed by this ruling, but refuse to let World Athletics drug me or stop me from being who I am,” she said. “Excluding female athletes or endangering our health solely because of our natural abilities puts World Athletics on the wrong side of history. I will continue to fight for the human rights of female athletes, both on the track and off the track, until we can all run free the way we were born.” The South African was almost unstoppable until World Athletics implemented a new policy for DSD athletes, including Semenya, that compelled them to reduce their testosterone levels to less than 5 nmol/L if they wanted to compete in elite events between 400m and a mile. © 2020 Guardian News & Media Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27462 - Posted: 09.09.2020

by Chloe Williams A new wireless device activates a mouse’s neurons as it navigates a cage with food, hiding places and other mice, allowing researchers to study social behavior in a realistic environment1. Experiments using this setup suggest that oxytocin has distinct effects in different contexts — which may be particularly important as researchers explore the hormone’s value as a potential treatment for autism. The device makes use of optogenetics, a technique in which researchers use pulses of light to activate or silence neurons. Autism researchers have used the approach to manipulate neural circuits in mice, but traditional optogenetic devices involve a fiber-optic cable, which tethers the animal and interferes with social interactions. Other wireless devices have been able to activate neurons without a tether, but researchers have mostly used them to study social behavior involving just two mice interacting for only about 15 minutes in an otherwise empty cage — a scenario that fails to capture a full range of mouse behaviors2. The new wireless device, powered by two watch batteries, consists of a light-emitting diode attached to an optical fiber that is implanted into the brain. It has an on-off switch that allows researchers to control it remotely using a magnet placed inside the cage. Using this setup, researchers can modulate brain activity in a group of mice as they roam for days through a cage that has hiding places, platforms, a nest, food and water. The device’s designers tested it in mice engineered to express light-sensitive proteins in part of the hypothalamus. This region produces the hormone oxytocin, generally thought to reduce aggression and enhance social bonds. When delivered as a nasal spray, it improves social skills in some people with autism. © 2020 Simons Foundation

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27369 - Posted: 07.16.2020

By Gretchen Reynolds Exercise may help change exercisers’ brains in surprising ways, according to a new study of physical activity and brain health. The study, which included both mice and people, found that exercise prompts the liver to pump out a little-known protein, and that chemically upping the levels of that protein in out-of-shape, elderly animals rejuvenates their brains and memories. The findings raise provocative questions about whether the brain benefits of exercise might someday be available in a capsule or syringe form — essentially “exercise in a pill.” We already have considerable evidence, of course, that physical activity protects brains and minds from some of the declines that otherwise accompany aging. In past rodent studies, animals that ran on wheels or treadmills produced more new neurons and learned and remembered better than sedentary mice or rats. Similarly, older people who took up walking for the sake of science added tissue volume in portions of their brains associated with memory. Even among younger people, those who were more fit than their peers tended to perform better on cognitive tests. But many questions remain unanswered about how, at a cellular level, exercise remodels the brain and alters its function. Most researchers suspect that the process involves the release of a cascade of substances inside the brain and elsewhere in the body during and after exercise. These substances interact and ignite other biochemical reactions that ultimately change how the brain looks and works. But what the substances are, where they originate and how they meet and mingle has remained unclear. So, for the new study, which was published this month in Science, researchers at the University of California, San Francisco, and other institutions decided to look inside the minds and bloodstreams of mice. In past research from the same lab, the scientists had infused blood from young mice into older ones and seen improvements in the aging animals’ thinking. It was like “transferring a memory of youth through blood,” says Saul Villeda, a professor at U.C.S.F., who conducted the study with his colleagues Alana Horowitz, Xuelai Fan and others. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27368 - Posted: 07.16.2020

By Anna Goldfarb It’s understandable that you may be struggling to fall asleep these days. Our world has been turned upside down, so it is especially hard to unplug from the day and get the high-quality sleep your body needs. “Almost every single patient I’m speaking with has insomnia,“ said Dr. Alon Y. Avidan, a professor and vice chair in the department of neurology at the David Geffen School of Medicine at the University of California, Los Angeles, and director of the U.C.L.A. Sleep Disorders Center. “Especially now with Covid-19, we have an epidemic of insomnia. We call it Covid-somnia.” An increase in anxiety in both children and adults is affecting our ability to fall asleep. Additionally, our lifestyles have changed drastically as people observe sheltering in place guidelines. With more people staying indoors, it can mean they are not getting enough light exposure. “Without light exposure in the morning,” Dr. Avidan said, people “lose the circadian cues that are so fundamentally important in setting up appropriate and normal sleep-wake time.” There are nonmedical ways to help you sleep better: Meditation, turning off screens early in the night, warm showers and cool bedrooms can help your body rest better. But if these options don’t work, or if you are ready for the next step, you may have considered trying melatonin supplements. These pills are commonplace enough that you have most likely heard of them and seen them in your local pharmacy. Here’s what you need to know about the pros and cons of using melatonin supplements for sleeping difficulties. What is melatonin? Melatonin is a hormone that helps regulate sleep timing. It is produced in the pea-size pineal gland, which is nestled in the middle of your brain and syncs melatonin production with the rising and setting of the sun. According to the National Sleep Foundation, the gland remains inactive during the day but switches on around 9 p.m. (when it’s generally dark) to flood the brain with melatonin for the next 12 hours. © 2020 The New York Times Company

Keyword: Sleep; Biological Rhythms
Link ID: 27360 - Posted: 07.14.2020

By Yasmin Anwar, Media Relations Stephen Glickman, a pioneer in behavioral endocrinology and founder of the world’s first colony of captive spotted hyenas — he raised generations of them in a UC Berkeley research facility — died at his home in Berkeley on May 22 from pancreatic cancer. He was 87. A professor emeritus of psychology and of integrative biology, whose lifelong bond with animals began during his boyhood near the Bronx Zoo in New York, Glickman joined the UC Berkeley faculty in 1968. Over the next five decades, he conducted studies of creatures great and small, authoring more than 100 research papers. His sharp intellect, warm wit and overall lovability engaged peers and protégés in scientific and social justice pursuits, colleagues said. “Steve was a giant in the field of animal behavior,” said UC Berkeley psychology chair Ann Kring. “He studied a wide variety of species in the wild, at the zoo and, perhaps most famously, at the field station where he conducted work with hyenas for more than 30 years.” Glickman’s standout legacy is his ardent stewardship of a colony of spotted hyenas at UC Berkeley’s Field Station for the Study of Behavior, Ecology and Reproduction. The hyena compound in the Berkeley hills, above the campus, closed in 2014 when funding dried up, but not before yielding seminal discoveries about endocrinology, fertility and other medical conditions that affect humans. Hormone-driven matriarchy By studying female hyenas, who use a long, phallic clitoris, instead of a vagina, for mating and giving birth, Glickman and fellow researchers found that high levels of androgens produced in their ovaries masculinized their sex organs and boosted their aggression and dominance in the pack. Copyright © 2020 UC Regents; all rights reserved

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 27292 - Posted: 06.09.2020