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by Bethany Brookshire The clearish lump looks like some bizarre, translucent gummy candy that might have once been piña colada flavored. But this is something you definitely don’t want to eat. That see-through blob was once a mouse. In the Aug. 14 Cell, scientists at Caltech detail the difficult series of methods required to make small animals such as mice and rats completely translucent. Scientists have been trying to clear tissue for better observation since the 1800s, and, as with all science, the new techniques build on many previous experiments done in a variety of labs. The techniques make it possible to capture images both beautiful and gross. And the procedure will teach scientists more about anatomy than ever before. If you want to render an animal transparent, you first have to overcome a solid problem: lipids. This group includes molecules essential to life, such as fats, cholesterols, waxes and steroids. Lipids form the membranes that surround our cells, the hormones that make us grow and reproduce and much, much more. But lipids have a problem. You can’t see through them. So to render an organism transparent, you need to remove the lipids. Bin Yang and colleagues in Viviana Gradinaru’s lab at Caltech used detergents to dissolve the lipids. The technique is based on CLARITY, a method that Gradinaru helped to develop in Karl Deisseroth’s lab at Stanford. Scientists there rendered a mouse brain transparent using CLARITY. Gradinaru explains that for a clear organ, dissolving lipids alone alone isn’t enough. “Without lipids the tissue would just collapse, so we need to maintain the structure of the tissue,” she says. © Society for Science & the Public 2000 - 2013
Keyword: Brain imaging
Link ID: 19963 - Posted: 08.16.2014
By Kate Yandell Researchers have accumulated detailed knowledge of the neurons that drive male fruit flies’ mating behaviors. But the neurons that prompt females to respond—or not—to male overtures have been less-studied. Three papers published today (July 2) in Neuron and Current Biology begin to change that. They identify sets of neurons in female fruit flies that help process mating signals, modulate the insects’ receptivity to male courtship, and drive mating behavior. “These three groups independently identified important neuronal groups [that] are positioned in different points in the neuronal circuitry for regulating female receptivity,” said Daisuke Yamamoto, a behavioral geneticist at Tohoku University in Japan who was not involved in any of the studies. “We’ve had access to the male circuitry for a while now, and that’s turning out to be a really interesting way to study how behavior works,” said Jennifer Bussell, whose work as a PhD student at Rockefeller University contributed to the Current Biology paper. “Having that complementary circuit in the female can only provide more fodder for interesting experiments.” Female fruit flies’ mating behaviors depend on their reproductive state. They become receptive to mating as they mature, but become less receptive to males’ advances immediately after mating. If a female fruit fly is receptive to mating, she responds to male pheromones and courtship songs by engaging in a behavior called pausing, where she stops in her tracks near males so they can mount her and she opens her vaginal plates—hard coverings that protect her reproductive tract. © 1986-2014 The Scientist
Keyword: Sexual Behavior
Link ID: 19962 - Posted: 08.16.2014
By Lenny Bernstein Comedian Robin Williams was grappling with severe depression when he committed suicide Monday, and on Thursday we learned that he also was in the early stages of Parkinson's disease. Sadly, the two conditions are often found together. In a 2012 study conducted by the National Parkinson Foundation, 61 percent of 5,557 Parkinson's patients surveyed reported that they also suffered from depression, with symptoms that ranged from mild to severe. Both conditions are associated with a shortage of dopamine, a neurotransmitter that helps regulate movement and control the brain's pleasure center. "Dopamine is a feel-good chemical. If you are low in dopamine, you are not going to feel so good," said Joyce Oberdorf, president and CEO of the National Parkinson Foundation. "There are [also] other neurotransmitters that can be low." A separate study published Friday found that newly-diagnosed Parkinson's patients have higher rates of depression, anxiety, fatigue, and apathy than a control group of people without Parkinson's. Researchers from the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania found that 13.9 percent of patients had symptoms of depression when they were diagnosed with Parkinson's, a proportion that rose to 18.7 percent after 24 months. Just 6.6 percent of people without the disease had depression, and that dropped to just 2.4 percent after 24 months. Despite their depressive symptoms, most of the Parkinson's patients who also had that condition were not treated with anti-depressants at any point in the two-year study. The findings were published in the journal Neurology.
By Rebecca Boyle Like a dog wagging its tail in anticipation of treats to come, dolphins and belugas squeal with pleasure at the prospect of a fish snack, according to a new study. It’s the first direct demonstration of an excitement call in these animals, says Peter Madsen, a biologist at Aarhus University in Denmark who was not involved in the study. To hunt and communicate, dolphins and some whale species produce a symphony of clicks, whistles, squeaks, brays, and moans. Sam Ridgway, a longtime marine biologist with the U.S. Navy’s Marine Mammal Program, says he heard distinctive high-pitched squeals for the first time in May 1963 while training newly captured dolphins at the Navy’s facility in Point Mugu, California. “We were throwing fish in, and each time they would catch a fish, they would make this sound,” he says. He describes it as a high-pitched “eeee,” like a child squealing in delight. Ridgway and his collaborators didn’t think much of the sound until later in the 1960s, when dolphins trained to associate a whistle tone with a task or behavior also began making it. Trainers teach animals a task by rewarding them with a treat and coupling it with a special noise, like a click or a whistle. Eventually only the sound is used, letting the animal know it will get a treat later. The whistle was enough to provoke a victory squeal, Ridgway says. Meanwhile, beluga whales would squeal after diving more than 600 meters to switch off an underwater speaker broadcasting tones. “As soon as the tone went off, they would make this same sound,” Ridgway says, “despite the fact that they’re not going to get a reward for five minutes.” He also heard the squeal at marine parks in response to trainers’ whistles. © 2014 American Association for the Advancement of Science.
Greta Kaul It was a rainy day, and earthworms wriggled out of the ground and began to arrange themselves on the pavement as Julian Plumadore walked to his community college zoology class in 1991. They spelled out messages only he could read. "I was very frightened to be a custodian of that kind of cosmic information and be able to do absolutely nothing about it," Plumadore said. Other times, there were voices - demons screaming - telling him he was going to hell. Plumadore was eventually diagnosed as having schizoaffective disorder, a psychosis that combines the hallucinations of schizophrenia with a mood disorder like depression. People with psychotic disorders, of which schizophrenia is the most severe, have hallucinations, like the voices Plumadore was hearing, that are divorced from reality. Now, a Stanford researcher suggests that the voices he experienced might have been different if he had grown up somewhere other than the U.S. If he were from India, he might have heard family members telling him to do household chores. If he were from Ghana, he might have heard the voice of God guiding him. For a study published in June, Tanya Luhrmann, a Stanford anthropologist, and other researchers interviewed 60 people who met the criteria for schizophrenia: 20 from in and around San Mateo, 20 from India and 20 from Ghana. Though the patients heard both positive and negative voices no matter where they were from, those in India and in Ghana tended to have less negative experiences than Americans: They could more often identify who was talking to them and had less violent hallucinations. Though the study isn't conclusive, Luhrmann believes the differences in voice-hearing between cultures may be a clue into how social expectations and environment shape the way people hear those imaginary voices. © 2014 Hearst Communications, Inc.
Hearing voices is an experience that is very distressing for many people. Voices – or “auditory verbal hallucinations” – are one of the most common features of schizophrenia and other psychiatric disorders. But for a small minority of people, voice-hearing is a regular part of their lives, an everyday experience that isn’t associated with being unwell. It is only in the past 10 years that we have begun to understand what might be going on in “non-clinical” voice-hearing. Most of what we know comes from a large study conducted by Iris Sommer and colleagues at UMC Utrecht in the Netherlands. In 2006 they launched a nationwide attempt to find people who had heard voices before but didn’t have any sort of psychiatric diagnosis. From an initial response of over 4,000 people, they eventually identified a sample of 103 who heard voices at least once a month, but didn’t have psychosis. Their voice-hearing was also not caused by misuse of drugs or alcohol. Twenty-one of the participants were also given an MRI scan. When this group was compared with voice-hearers who did have psychosis, many of the same brain regions were active for both groups while they were experiencing auditory hallucinations, including the inferior frontal gyrus (involved in speech production) and the superior temporal gyrus (linked to speech perception). Subsequent studies with the same non-clinical voice-hearers have also highlighted differences in brain structure and functional connectivity (the synchronisation between different brain areas) compared with people who don’t hear voices. These results suggest that, on a neural level, the same sort of thing is going on in clinical and non-clinical voice-hearing. We know from first-person reports that the voices themselves can be quite similar, in terms of how loud they are, where they are coming from, and whether they speak in words or sentences. © 2014 Guardian News and Media Limited
By Jen Christiansen I threw down a bit of a challenge last month at the Association of Medical Illustrators Conference in Minnesota. But first, I had to—somewhat unexpectedly—accept some challenges presented by others. And face the reality that some of us simply do not have the constitution of an anatomist. I love classic anatomical illustrations such as the vintage works of Andreas Vesalius and the more modern stylings of Frank Netter. And on that front, this conference definitely delivered. Talks by Daniel Garrison and Francine Netter were drool-worthy, and I snapped photos of quickly advancing slides presented by W. Bruce Fye on the history of the illustrated heart, so I could reverse-image search them later and spend more time checking out the details and context. Videos of Robert Beverly Hale’s Art Students League lectures on anatomy charmed me (as presented by Glen Hintz), as well as new videos of clean architectural microstructures like the inner ear, presented by Robert Acland. I had to make myself walk quickly by one vendor table to avoid blowing my book budget for the year (and then some) on an impulse buy of Vesalius’ 1543 De Humani Corporis Fabrica, newly translated to English. But I averted my gaze when surgeons presented on the topic of facial transplantation and skull reconstruction. Shoot, I couldn’t even look at the screen through the entirety of a fascinating talk by Elizabeth Weissbrod and Valerie Henry on creating and using virtual and prosthetic simulations for military emergency response training. I avoided the hands-on human cadaveric dissection workshop sessions, telling myself and others that my travel schedule would simply not allow me to get to the Mayo Clinic in Rochester, Minn., early enough to participate or observe. © 2014 Scientific American
Keyword: Brain imaging
Link ID: 19957 - Posted: 08.14.2014
The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.
By NICHOLAS BAKALAR A new study reports that caffeine intake is associated with a reduced risk for tinnitus — ringing or buzzing in the ears. Researchers tracked caffeine use and incidents of tinnitus in 65,085 women in the Nurses’ Health Study II. They were 30 to 34 and without tinnitus at the start of the study. Over the next 18 years, 5,289 developed the disorder. The women recorded their use of soda, coffee and tea (caffeinated and not), as well as intake of candy and chocolate, which can contain caffeine. The results appear in the August issue of The American Journal of Medicine. Compared with women who consumed less than 150 milligrams of caffeine a day (roughly the amount in an eight-ounce cup of coffee), those who had 450 to 599 milligrams a day were 15 percent less likely to have tinnitus, and those who consumed 600 milligrams or more were 21 percent less likely. The association persisted after controlling for other hearing problems, hypertension, diabetes, use of anti-inflammatory Nsaid drugs, a history of depression and other factors. Decaffeinated coffee consumption had no effect on tinnitus risk. “We can’t conclude that caffeine is a cure for tinnitus,” said the lead author, Dr. Jordan T. Glicksman, a resident physician at the University of Western Ontario. “But our results should provide some assurance to people who do drink caffeine that it’s reasonable to continue doing so.” © 2014 The New York Times Company
Link ID: 19955 - Posted: 08.14.2014
by Catherine Brahic Think crayfish and you probably think supper, perhaps with mayo on the side. You probably don't think of their brains. Admittedly, crayfish aren't known for their grey matter, but that might be about to change: they can grow new brain cells from blood. Humans can make new neurons, but only from specialised stem cells. Crayfish, meanwhile, can convert blood to neurons that resupply their eyestalks and smell circuits. Although it's a long way from crayfish to humans, the discovery may one day help us to regenerate our own brain cells. Olfactory nerves are continuously exposed to damage and so naturally regenerate in many animals, from flies to humans, and crustaceans too. It makes sense that crayfish have a way to replenish these nerves. To do so, they utilise what amounts to a "nursery" for baby neurons, a little clump at the base of the brain called the niche. In crayfish, blood cells are attracted to the niche. On any given day, there are a hundred or so cells in this area. Each cell will split into two daughter cells, precursors to full neurons, both of which migrate out of the niche. Those that are destined to be part of the olfactory system head to two clumps of nerves in the brain called clusters 9 and 10. It's there that the final stage of producing new smell neurons is completed. © Copyright Reed Business Information Ltd.
|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American
Link ID: 19953 - Posted: 08.13.2014
By GRETCHEN REYNOLDS Regular exercise may alter how a person experiences pain, according to a new study. The longer we continue to work out, the new findings suggest, the greater our tolerance for discomfort can grow. For some time, scientists have known that strenuous exercise briefly and acutely dulls pain. As muscles begin to ache during a prolonged workout, scientists have found, the body typically releases natural opiates, such as endorphins, and other substances that can slightly dampen the discomfort. This effect, which scientists refer to as exercise-induced hypoalgesia, usually begins during the workout and lingers for perhaps 20 or 30 minutes afterward. But whether exercise alters the body’s response to pain over the long term and, more pressing for most of us, whether such changes will develop if people engage in moderate, less draining workouts, have been unclear. So for the new study, which was published this month in Medicine & Science in Sports & Exercise, researchers at the University of New South Wales and Neuroscience Research Australia, both in Sydney, recruited 12 young and healthy but inactive adults who expressed interest in exercising, and another 12 who were similar in age and activity levels but preferred not to exercise. They then brought all of them into the lab to determine how they reacted to pain. Pain response is highly individual and depends on our pain threshold, which is the point at which we start to feel pain, and pain tolerance, or the amount of time that we can withstand the aching, before we cease doing whatever is causing it. © 2014 The New York Times Company
Keyword: Pain & Touch
Link ID: 19952 - Posted: 08.13.2014
|By Piercarlo Valdesolo In the summer of 2009 I tried to cure homemade sausages in my kitchen. One of the hazards of such a practice is preventing the growth of undesirable molds and diseases such as botulism. My wife was not on board with this plan, skeptical of my ability to safely execute the procedure. And so began many weeks of being peppered with warnings, relevant articles and concerned looks. When the time came for my first bite, nerves were high. My throat itched. My heart raced. My vision blurred. I had been botulized! Halfway through our walk to the hospital I regained my composure. Of course I had not been instantaneously struck by an incredibly rare disease that, by the way, takes at least 12 hours after consumption to manifest and does not share many symptoms with your garden variety anxiety attack. My experience had been shaped by my mindset. A decade of learning about the psychological power of expectations could not inoculate me from its effect. Psychologists know that beliefs about how experiences should affect us can bring about the expected outcomes. Though these “placebo effects” have primarily been studied in the context of pharmaceutical interventions (e.g. patients reporting pain relief after receiving saline they believed to be an analgesic), recent research has shown their strength in a variety of domains. Tell people that their job has exercise benefits and they will lose more weight than their coworkers who had no such belief. Convince people of a correlation between athleticism and visual acuity and they will show better vision after working out . Trick people into believing they are consuming caffeine and their vigilance and cognitive functioning increases. Some evidence shows that such interventions can even mitigate the negative effects of other experiences. For example, consuming placebo caffeine alleviates the cognitive consequences of sleep deprivation. © 2014 Scientific American
By EDWARD LARKIN and IRENE HURFORD PHILADELPHIA — A FEW months ago, a patient came to our hospital, seeking help. One of us, Edward, was on the team that treated him. He was pleasant, if slightly withdrawn, and cogent. He was a college graduate in his 20s and had recently been fired from his job as a high school math teacher, because of unexpected absences. He had come to believe that government agents were conspiring against him, and he had taken to living out of a truck and sleeping in different parking lots. By the time he came to us, he was exhausted. A diagnosis became clear: he had schizophrenia. We admitted him to the hospital, and after a few days, with his symptoms under control, we released him. Unfortunately, we prescribed a medication for him that could cause significant, permanent harm, instead of an equally effective drug with milder side effects — all because he was uninsured. Schizophrenia, which affects 1 percent of the population and emerges in the late teens to early 20s, is deeply misunderstood. People who suffer from it are often suspected of being dangerous, but this is not usually the case, and antipsychotic drugs are very effective. Our patient was exactly the kind of person who, with the right treatment, could have weakened the stigma surrounding schizophrenia. Antipsychotic drugs fall into two classes: the older ones, like Haldol, and newer ones, like Abilify and Latuda. Both classes are equally effective at treating some of the worst symptoms of schizophrenia, specifically the hallucinations, delusions and paranoia that cause social alienation. (They’re not effective for treating “negative symptoms,” like low motivation.) But the older drugs can cause a multitude of serious side effects, including a potentially devastating one called tardive dyskinesia. This condition involves unsettling, animalistic smacking and wagging of the lips and tongue. At its extreme, it can affect the entire body. It occurs in 20 percent or more of patients who take the drugs long-term, and it tends to start so mildly that patients can’t identify it in time to stop taking the drugs. It is often irreversible. © 2014 The New York Times Company
Link ID: 19950 - Posted: 08.13.2014
Sara Reardon When the states of Colorado and Washington voted to legalize marijuana in 2012, the abrupt and unprecedented policy switch sent the US National Institute on Drug Abuse (NIDA) into what its director Nora Volkow describes as “red alarm”. Although marijuana remained illegal for people under the age of 21, the drug’s increased availability and growing public acceptance suggested that teenagers might be more likely to try it (see ‘Highs and lows’). Almost nothing is known about whether or how marijuana affects the developing adolescent brain, especially when used with alcohol and other drugs. The new laws, along with advances in brain-imaging technology, convinced Volkow to accelerate the launch of an ambitious effort to follow 10,000 US adolescents for ten years in an attempt to determine whether marijuana, alcohol and nicotine use are associated with changes in brain function and behaviour. At a likely cost of more than US$300 million, it will be the largest longitudinal brain-imaging study of adolescents yet. Researchers are eager to study a poorly understood period of human development — but some question whether it is possible to design a programme that will provide useful information about the effects of drugs. “It’s definitely an idea that’s overdue,” says Deanna Barch, a psychologist at Washington University in St. Louis, Missouri. “The downside is it’s a lot of eggs in one basket.” © 2014 Nature Publishing Group,
By MICHAEL CIEPLY and BROOKS BARNES LOS ANGELES — Peering through his camera at Robin Williams in 2012, the cinematographer John Bailey thought he glimpsed something not previously evident in the comedian’s work. They were shooting the independent film “The Angriest Man in Brooklyn,” and Mr. Williams was playing a New York lawyer who, facing death, goes on a rant against the injustice and banality of life. His performance, Mr. Bailey said Tuesday, was a window into the “Swiftian darkness of Robin’s heart.” The actor, like his character, was raging against the storm. That defiance gave way on Monday to the personal demons that had long tormented Mr. Williams. With his suicide at age 63, Mr. Williams forever shut the window on a complicated soul that was rarely visible through the cracks of an astonishingly intact career. Given his well-publicized troubles with depression, addiction, alcoholism and a significant heart surgery in 2009, Mr. Williams should have had a résumé filled with mysterious gaps. Instead, he worked nonstop. At the very least — if his life had followed the familiar script of troubled actors — there would have been whispers of on-set antics: lateness, forgotten lines, the occasional flared temper. Not so with Mr. Williams. “He was ready to work, he was the first one on the set,” said Mr. Bailey, speaking of Mr. Williams’s contribution to “The Angriest Man in Brooklyn,” of which he was the star. “Robin was always 1,000 percent reliable,” said a senior movie agent, speaking on the condition of anonymity to conform to the wishes of Mr. Williams’s family. “He was almost impossibly high functioning.” As Hollywood struggled on Tuesday to understand how Mr. Williams — effervescent in the extreme — could take his own life, authorities released details of his death. A clothed Mr. Williams hanged himself with a belt from a door frame in his bedroom in Tiburon, Calif., according to Lt. Keith Boyd, assistant deputy chief coroner for Marin County. © 2014 The New York Times Company
Link ID: 19948 - Posted: 08.13.2014
By Lenny Bernstein, Lena H. Sun and Sandhya Somashekhar Suicides are the 10th-leading cause of death in the United States and eighth among people in the 55- to 64-year-old age group. Comedian Robin Williams, who died Monday of an apparent suicide, was 63. In 2010, 38,364 people died this way. Many suicides are the result of undiagnosed or untreated depression, often masked by self-medicating behaviors such as alcohol and drug use. Though we don’t yet know the exact circumstances of Williams’s death, we do know that he long battled addictions to cocaine and alcohol and, according to his publicist, was struggling with “severe depression.” But unlike many people, Williams had the resources and the motivation to seek treatment, at least for his addictions. According to this report, he had undergone rehab at the famed Hazelden Addiction Treatment Center in Minnesota two months ago, and had sought treatment in 2006 when he began drinking again after 20 years of sobriety. How, then, do we explain the death of someone who appeared to recognize the danger he faced and was trying to address it? Here are some thoughts: • Suicides are often impulsive acts: People who kill themselves are not thinking clearly, have trouble solving problems and weigh risks differently from us, Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention, told To Your Health in March. If thwarted in their first attempt, they often do not try again immediately, she said.
Jia You Premature babies are more likely to produce piercing cries than their full-term peers are, researchers report online today in Biology Letters. Scientists have studied infant crying as a noninvasive way to assess how well a baby’s nervous system develops. Previous research of full-term babies indicates that an abnormally high pitch is associated with disturbances in an infant’s metabolism and neurological development. The team recorded spontaneous crying in preterm babies and full-term babies of the same age and compared the pitch of their sobs. They found that preterm babies whimper in a shriller voice, but not because they are smaller in size or grew at a slower rate in their mothers’ wombs. Instead, the researchers suspect the high pitch could reflect lower levels of activities in a premature baby’s vagal nerve, which extends from the brain stem to the abdomen. Vagal nerve activities are believed to decrease tension in the vocal cords, thus producing a lower pitch. Previous studies show that giving preterm babies massage therapies can stimulate their vagal activities, improve their ingestion, and help them gain weight. © 2014 American Association for the Advancement of Science
Keyword: Development of the Brain
Link ID: 19946 - Posted: 08.13.2014
James Gorman Deep in the mouse brain, scientists recently found that a very small network of cells, a few thousand at most, turns appetite on and off. They used the most sophisticated of modern techniques, but as has often happened in science — witness penicillin, Velcro and Viagra — the researchers discovered something they weren’t looking for. “This was an accidental discovery,” said David Anderson, of the California Institute of Technology, the senior scientist on the team that reported the finding, in Nature Neuroscience. The discovery may eventually lead to a better understanding and treatment of eating disorders. The surprise and drama of the finding are immediately clear, however, in lab videos. A mouse busily munches lab chow until a light signal is sent to its brain, and the mouse wanders off, no longer interested in food. His lab had previously studied this small group of neurons, in a part of the brain called the amygdala. That earlier research was on fear, an emotion strongly associated with the amygdala in both mice and humans. As a technique called optogenetics became more and more refined, he said, it seemed worth revisiting the neurons with this new tool. Optogenetics requires genetic manipulation of specific cells to make them sensitive to light in a certain wavelength, in this case blue light. Then fiber-optic cables are inserted into the brain, and when the light is turned on, neurons can be activated or turned off. Researchers in Dr. Anderson’s lab, including Haijiang Cai, a postdoctoral researcher and a co-author of the report, prepared the mice and conducted the experiment with the entirely unexpected result. © 2014 The New York Times Company
Link ID: 19945 - Posted: 08.12.2014
By Rachel Feltman Bioengineers have created the most realistic fake brain tissue ever – and it’s built like a jelly doughnut. The 3-D tissue, described in a paper published Monday in Proceedings of the National Academy of Sciences, is so structurally similar to a real rat brain (a common substitute for human brains in the lab) that it could help scientists answer longstanding questions about brain injuries and disease. Currently, the best way to study brain tissue is to grow neurons in a petri dish, but those neurons can only be grown flat. A real brain contains a complicated structure of 3-D tissue. Simply giving the neurons room to grow in three dimensions didn’t prove successful: While neurons will grow into more complicated structures in the right kind of gel, they don’t survive very long or mimic the structure of a real brain. Led by David Kaplan, the director of the Tissue Engineering Resource Center at Tufts University, researchers developed a new combination of materials to mimic the gray and white matter of the brain. The new model relies on a doughnut-shaped, spongy scaffold made of silk proteins with a collagen-based gel at the center. The outer scaffold layer, which is filled with rat neurons, acts as the grey matter of the brain. As the neurons grew networks throughout the scaffold, they sent branches out across the gel-filled center to connect with neurons on the other side. And that configuration is about as brain-like as lab-grown tissue can get. The basic structure can be reconfigured, too.