By Meeri Kim, Many of us find ourselves swimming along in the tranquil sea of life when suddenly a crisis hits — a death in the family, the loss of a job, a bad breakup. Some power through and find calm waters again, while others drown in depression. Scientists continue to search for the underlying genes and neurobiology that dictate our reactions to stress. Now, a study using mice has found a switch-like mechanism between resilience and defeat in an area of the brain that plays an important role in regulating emotions and has been linked with mood and anxiety disorders. (Bo Li/Cold Spring Harbor Laboratory) - Researchers at Cold Spring Harbor Laboratory identify the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (top, green image) become hyperactive in depressed mice. The bottom panel is close-up of above image - yellow indicates activation. The team showed that this enhanced activity causes depression. After artificially enhancing the activity of neurons in that part of the brain — the medial prefrontal cortex — mice that previously fought to avoid electric shocks started to act helpless. Rather than leaping for an open escape route, they sat in a corner taking the pain — presumably out of a belief that nothing they could do would change their circumstances. “This helpless behavior is quite similar to what clinicians see in depressed individuals — an inability to take action to avoid or correct a difficult situation,” said study author and neuroscientist Bo Li of the Cold Spring Harbor Laboratory in New York. The results were published online May 27 in the Journal of Neuroscience. © 1996-2014 The Washington Post

Keyword: Depression
Link ID: 19704 - Posted: 06.06.2014

By ANNA NORTH The “brain” is a powerful thing. Not the organ itself — though of course it’s powerful, too — but the word. Including it in explanations of human behavior might make those explanations sound more legitimate — and that might be a problem. Though neuroscientific examinations of everyday experiences have fallen out of favor somewhat recently, the word “brain” remains popular in media. Ben Lillie, the director of the science storytelling series The Story Collider, drew attention to the phenomenon last week on Twitter, mentioning in particular a recent Atlantic article: “Your Kid’s Brain Might Benefit From an Extra Year in Middle School.” In the piece, Jessica Lahey, a teacher and education writer, examined the benefits of letting kids repeat eighth grade. Mr. Lillie told Op-Talk the word “brain” could take the emphasis off middle-school students as people: The piece, he said, was “not ignoring the fact that the middle schooler (in this case) is a person, but somehow taking a quarter-step away by focusing on a thing we don’t really think of as human.” The New York Times isn’t immune to “brain”-speak — in her 2013 project “Brainlines,” the artist Julia Buntaine collected all Times headlines using the word “brain” since 1851. She told Op-Talk in an email that “the number of headlines about the brain increased exponentially since around the year 2000, where some years before there were none at all, after that there were at least 30, 40, 80 headlines.” Adding “brain” to a headline may make it sound more convincing — some research shows that talking about the brain has measurable effects on how people respond to scientific explanations. In a 2008 study, researchers found that adding phrases like “brain scans indicate” to explanations of psychological concepts like attention made those explanations more satisfying to nonexpert audiences. Perhaps disturbingly, the effect was greatest when the explanations were actually wrong. © 2014 The New York Times Company

Keyword: Miscellaneous
Link ID: 19703 - Posted: 06.06.2014

Neil Levy Can human beings still be held responsible in the age of neuroscience? Some people say no: they say once we understand how the brain processes information and thereby causes behaviour, there’s nothing left over for the person to do. This argument has not impressed philosophers, who say there doesn’t need to be anything left for the person to do in order to be responsible. People are not anything over and above the causal systems involved in information processing, we are our brains (plus some other, equally physical stuff). We are responsible if our information processing systems are suitably attuned to reasons, most philosophers think. There are big philosophical debates concerning what it takes to be suitably attuned to reasons, and whether this is really enough for responsibility. But I want to set those debates aside here. It’s more interesting to ask what we can learn from neuroscience about the nature of responsibility and about when we’re responsible. Even if neuroscience doesn’t tell us that no one is ever responsible, it might be able to tell us if particular people are responsible for particular actions. A worthy case study Consider a case like this: early one morning in 1987, a Canadian man named Ken Parks got up from the sofa where he had fallen asleep and drove to his parents’-in-law house. There he stabbed them both before driving to the police station, where he told police he thought he had killed someone. He had: his mother-in-law died from her injuries. © 2010–2014, The Conversation Trust (UK)

Keyword: Consciousness; Emotions
Link ID: 19702 - Posted: 06.06.2014

By Sadie Dingfelder Want to become famous in the field of neuroscience? You could go the usual route, spending decades collecting advanced degrees, slaving away in science labs and publishing your results. Or you could simply fall victim to a freak accident. The stars of local science writer Sam Kean’s new book, “The Tale of the Dueling Neurosurgeons,” (which he’ll discuss Saturday at Politics and Prose) took the latter route. Be it challenging the wrong guy to a joust, spinning out on a motorcycle, or suffering from a stroke, these folks sustained brain injuries with bizarre and fascinating results. One man, for instance, lost the ability to identify different kinds of animals but had no trouble naming plants and objects. Another man lost his short-term memory. The result? A diary filled with entries like: “I am awake for the very first time.” “Now, I’m really awake.” “Now, I’m really, completely awake.” Unfortunate mishaps like these have advanced our understanding of how the gelatinous gray mass that (usually) stays hidden inside our skulls gives rise to thoughts, feelings and ideas, Kean says. “Traditionally, every major discovery in the history of neuroscience came about this way,” he says. “We had no other way of looking at the brain for centuries and centuries, because we didn’t have things like MRI machines.” Rather than covering the case studies textbook-style, Kean provides all the gory details. Consider Phineas Gage. You may remember from Psych 101 that Gage, a railroad worker, survived having a metal rod launched through his skull. You might not know, however, that one doctor “shaved Gage’s scalp and peeled off the dried blood and gelatinous brains. He then extracted skull fragments from the wound by sticking his fingers in from both ends, Chinese-finger-trap-style,” as Kean writes in his new book. © 1996-2014 The Washington Post

Keyword: Learning & Memory; Attention
Link ID: 19701 - Posted: 06.06.2014

By Ian Randall The human tongue may have a sixth sense—and no, it doesn’t have anything to do with seeing ghosts. Researchers have found that in addition to recognizing sweet, sour, salty, savory, and bitter tastes, our tongues can also pick up on carbohydrates, the nutrients that break down into sugar and form our main source of energy. Past studies have shown that some rodents can distinguish between sugars of different energy densities, while others can still tell carbohydrate and protein solutions apart even when their ability to taste sweetness is lost. A similar ability has been proposed in humans, with research showing that merely having carbohydrates in your mouth can improve physical performance. How this works, however, has been unclear. In the new study, to be published in Appetite, the researchers asked participants to squeeze a sensor held between their right index finger and thumb when shown a visual cue. At the same time, the participants’ tongues were rinsed with one of three different fluids. The first two were artificially sweetened—to identical tastes—but with only one containing carbohydrate; the third, a control, was neither sweet nor carb-loaded. When the carbohydrate solution was used, the researchers observed a 30% increase in activity for the brain areas that control movement and vision. This reaction, they propose, is caused by our mouths reporting that additional energy in the form of carbs is coming. The finding may explain both why diet products are often viewed as not being as satisfying as their real counterparts and why carbohydrate-loaded drinks seem to immediately perk up athletes—even before their bodies can convert the carbs to energy. Learning more about how this “carbohydrate sense” works could lead to the development of artificially sweetened foods, the researchers propose, “as hedonistically rewarding as the real thing.” © 2014 American Association for the Advancement of Science

Keyword: Chemical Senses (Smell & Taste)
Link ID: 19700 - Posted: 06.06.2014

By Jenny Graves The claim that homosexual men share a “gay gene” created a furor in the 1990s. But new research two decades on supports this claim – and adds another candidate gene. To an evolutionary geneticist, the idea that a person’s genetic makeup affects their mating preference is unsurprising. We see it in the animal world all the time. There are probably many genes that affect human sexual orientation. But rather than thinking of them as “gay genes,” perhaps we should consider them “male-loving genes.” They may be common because these variant genes, in a female, predispose her to mate earlier and more often and to have more children. Likewise, it would be surprising if there were not “female-loving genes” in lesbian women that, in a male, predispose him to mate earlier and have more children. We can detect genetic variants that produce differences between people by tracking traits in families that display differences. Patterns of inheritance reveal variants of genes (called “alleles”) that affect normal differences, such as hair color, or disease states, such as sickle cell anemia. Quantitative traits, such as height, are affected by many different genes, as well as environmental factors. It’s hard to use these techniques to detect genetic variants associated with male homosexuality partly because many gay men prefer not to be open about their sexuality. It is even harder because, as twin studies have shown, shared genes are only part of the story. Hormones, birth order and environment play roles, too.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 19699 - Posted: 06.06.2014

By Kelly Servick During the World Cup next week, there may be 1 minute during the opening ceremony when the boisterous stadium crowd in São Paulo falls silent: when a paraplegic young person wearing a brain-controlled, robotic exoskeleton attempts to rise from a wheelchair, walk several steps, and kick a soccer ball. The neuroscientist behind the planned event, Miguel Nicolelis, is familiar with the spotlight. His lab at Duke University in Durham, North Carolina, pioneered brain-computer interfaces, using surgically implanted electrodes to read neural signals that can control robotic arms. Symbolically, the project is a homecoming for Nicolelis. He has portrayed it as a testament to the scientific progress and potential of his native Brazil, where he founded and directs the International Institute of Neuroscience of Natal. The press has showered him with attention, and the Brazilian government chipped in nearly $15 million in support. But scientifically, the project is a departure. Nicolelis first intended the exoskeleton to read signals from implanted electrodes, but decided instead to use a noninvasive, EEG sensor cap. That drew skepticism from Nicolelis’s critics—and he has a few—that the system wouldn’t really be a scientific advance. Others have developed crude EEG-based exoskeletons, they note, and it will be impossible to tell from the demo how this system compares. A bigger concern is that the event could generate false hope for paralyzed patients and give the public a skewed impression of the field’s progress. © 2014 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 19698 - Posted: 06.06.2014

By JAMES GORMAN The National Institutes of Health set an ambitious $4.5 billion price tag on its part of President Obama’s Brain Initiative on Thursday, stamping it as an effort on the scale of the Human Genome Project. The goals of the Brain Initiative were clearly grand when Mr. Obama announced it a year ago — nothing less than developing and applying new technology to crack the toughest unsolved puzzles of how the brains of humans and animals function. The hope is to lay a foundation for future advances in the medical treatment of brain disorders. But the initiative began with $110 million budgeted for 2014, shared by three major entities: the National Science Foundation; the Defense Advanced Research Projects Agency; and the N.I.H., which has a $40 million share. By calling for such a major commitment, to be spread over 12 years, the institutes answered concerns among neuroscientists about the initial level of funding. “This is a realistic amount of money,” said Dr. Eric R. Kandel, director of the Kavli Institute for Brain Science at Columbia University, who, like some other neuroscientists, had been skeptical of what could be accomplished with the funding committed when the initiative was announced about a year ago. Gerald Rubin, the executive director of the Janelia Farm Research Campus in Virginia, also found that this budget request allayed some of his concerns, but not all. “I am much more concerned about convincing Congress to fund the Brain Initiative at this level,” he said. © 2014 The New York Times Company

Keyword: Brain imaging
Link ID: 19697 - Posted: 06.06.2014

Laura Spinney One day in 1991, neurologist Warren Strittmatter asked his boss to look at some bewildering data. Strittmatter was studying amyloid-β, the main component of the molecular clumps found in the brains of people with Alzheimer's disease. He was hunting for amyloid-binding proteins in the fluid that buffers the brain and spinal cord, and had fished out one called apolipoprotein E (ApoE), which had no obvious connection with the disease. Strittmatter's boss, geneticist Allen Roses of Duke University in Durham, North Carolina, immediately realized that his colleague had stumbled across something exciting. Two years earlier, the group had identified a genetic association between Alzheimer's and a region of chromosome 19. Roses knew that the gene encoding ApoE was also on chromosome 19. “It was like a lightning bolt,” he says. “It changed my life.” In humans, there are three common variants, or alleles, of the APOE gene, numbered 2, 3 and 4. The obvious step, Roses realized, was to find out whether individual APOE alleles influence the risk of developing Alzheimer's disease. The variants can be distinguished from one another using a technique called the polymerase chain reaction (PCR). But Roses had little experience with PCR, so he asked the postdocs in his team to test samples from people with the disease and healthy controls. The postdocs refused: they were busy hunting for genes underlying Alzheimer's, and APOE seemed an unlikely candidate. The feeling in the lab, recalls Roses, was that “the chief was off on one of his crazy ideas”. Roses then talked to his wife, Ann Saunders, a mouse geneticist who was skilled at PCR. She had just given birth to their daughter and was on maternity leave, so they struck a deal. “She did the experiments while I held the baby,” he says. Within three weeks, they had collected the data that would fuel a series of landmark papers showing that the APOE4 allele is associated with a greatly increased risk of Alzheimer's disease1. © 2014 Nature Publishing Group,

Keyword: Alzheimers; Genes & Behavior
Link ID: 19696 - Posted: 06.05.2014

A moderate dose of MDMA. commonly known as Ecstasy or Molly, that is typically nonfatal in cool, quiet environments can be lethal in rats exposed to conditions that mimic the hot, crowded, social settings where the drug is often used by people, a study finds. Scientists have identified the therapeutically-relevant cooling mechanism to enable effective interventions when faced with MDMA-induced hyperthermia. The study, publishing tomorrow in the Journal of Neuroscience, was conducted by researchers at the National Institute on Drug Abuse’s Intramural Research Program (NIDA IRP). NIDA is a part of the National Institutes of Health. While MDMA can have a range of adverse health effects, previous studies have shown that high doses of MDMA increase body temperature, while results with moderate doses were inconsistent. This has led some people to assume that the drug is harmless if taken in moderation. However, this study shows that in rats even moderate doses of MDMA in certain environments can be dangerous because it interferes with the body’s ability to regulate temperature. “We know that high doses of MDMA can sharply increase body temperature to potentially lead to organ failure or even death,” said NIDA Director Dr. Nora D. Volkow. “However, this current study opens the possibility that even moderate doses could be deadly in certain conditions.” It is impossible to predict who will have an adverse reaction even to a low dose of MDMA. However, in this study scientists gave the rats low to moderate doses that have been shown in past studies to not be fatal. They monitored the rats to determine drug-induced changes in brain and body temperature and in the body’s ability to cool itself through blood vessel dilation. When rats were alone and in a room-temperature environment, a moderate dose of MDMA modestly increased brain and body temperature and moderately diminished the rats’ ability to eliminate excessive heat. However, when researchers injected the same dose in rats that were either in a warmer environment or in the presence of another rat in the cage, brain temperature increased, causing death in some rats. These fatal temperature increases were because the drug interfered with the body’s ability to eliminate heat.

Keyword: Drug Abuse
Link ID: 19695 - Posted: 06.05.2014

By Charles Q. Choi Scientists have found a kind of brain cell in mice that can instruct stem cells to start making more neurons, according to a new study. In addition, they found that electrical signals could trigger this growth in rodents, raising the intriguing possibility that devices could one day help the human brain repair itself. The study appears in the journal Nature Neuroscience. We knew the brain can generate new neurons, a process known as neurogenesis, via neural stem cells. And neuroscientists knew these stem cells got their instructions from a variety of sources from chemicals in the bloodstream, for instance, and from cells in the structures that hold the cerebrospinal fluid that cushion the brain. Earlier research had suggested brain cells might also be able to command these stem cells to create neurons. Neuroscientist Chay Kuo at the Duke University School of Medicine in Durham, N.C., and his colleagues have now discovered such cells in mice. "It's really cool that the brain can tell stem cells to make more neurons," Kuo says. To begin their experiments, the researchers tested how well a variety of neurotransmitters performed at spurring mouse neural stem cells to produce new neurons; they found that a compound known as acetylcholine performed best. The team then discovered a previously unknown type of neuron that produces an enzyme needed to make acetylcholine. These neurons are found in a part of the adult mouse brain known as the subventricular zone, where neurogenesis occurs. ©2014 Hearst Communication, Inc

Keyword: Neurogenesis
Link ID: 19694 - Posted: 06.05.2014

By Denali Tietjen Meditation has long been known for its mental health benefits, but new research shows that just a few minutes of mindfulness can improve physical health and personal life as well. A recent study conducted by researchers at INSEAD and The Wharton School found that 15 minutes of mindful meditation can help you make better decisions. The research, published in the Association for Psychological Science’s journal Psychological Science, comes from four studies (varying in sample size from 69 to 178 adults) in which participants responded to sunk-cost scenarios at different degrees of mindful awareness. The results consistently showed that increased mindfulness decreases the sunk-cost bias. WOAH, hold the phone. What’s a sunk cost and what’s a sunk-cost bias?? Sunk cost is an economics term that psychologists have adopted. In economics, sunk costs are defined as non-recoverable investment costs like the cost of employee training or a lease on office space. In psychology, sunk costs are basically the same thing: The time and energy we put into our personal lives. Though we might not sit down with a calculator at the kitchen table when deciding who to take as our plus one to our second cousin’s wedding next weekend, we do a cost-benefit analysis every time we make a decision. And we take these sunk costs into account. The sunk-cost bias, then, is the tendency to allow sunk costs to overly influence current decisions. Mindfulness meditation can provide improved clarity, which helps you stay present and make better decisions, the study says. This protects you from that manipulative sunk-cost bias.

Keyword: Stress
Link ID: 19693 - Posted: 06.05.2014

by Bethany Brookshire We all respond to stress in different ways. Some of us work harder. Others drink more or eat our feelings. Sometimes we experience sleep loss, heart palpitations or sweats. When the stress dissipates, many of us go back to our daily lives, none the worse for wear. We are resilient. But some people find that stress is a first step on the way to a major depressive episode. It’s not quite clear what’s different between people who go back to normal after stress, and those who descend into depression. “One of the most important questions is, how do the brains of resilient animals (or humans) differ from those that are vulnerable to depression following stress?” asks John Morrison, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York. A new study from Minghui Wang and colleagues at Cold Spring Harbor Laboratory in New York provides a new hint. Mice with a depressive-like response to stress have stronger connections between neurons in the medial prefrontal cortex of the brain following the stress. Resilient mice show weaker connections. The mechanism could help scientists understand why some people respond to stress with depression, while others are able to shake it off. The prefrontal cortex is best known for its role in executive function — thought, memory, prediction and other tasks. But dysfunction in some areas of the cortex, particularly one called Brodmann area 25, has been linked with recurring major depressive disorder. Scientists have been electrically stimulating this area to relieve depression in patients. But researchers still don’t understand what makes this brain area important in depression, and how dysfunctions might occur. “I’ve had a long interest in the mechanism of human diseases like depression,” says study coauthor Bo Li, a cellular and behavioral neuroscientist at Cold Spring Harbor. “The idea has been to identify an area that is responsible, to link a mechanism in the brain to a behavior.” Wang, Li and their colleagues were especially interested in changes to the mouse prefrontal cortex following stress. © Society for Science & the Public 2000 - 2013.

Keyword: Stress; Depression
Link ID: 19692 - Posted: 06.04.2014

By GRETCHEN REYNOLDS If you are aiming to lose weight by revving up your exercise routine, it may be wise to think of your workouts not as exercise, but as playtime. An unconventional new study suggests that people’s attitudes toward physical activity can influence what they eat afterward and, ultimately, whether they drop pounds. For some time, scientists have been puzzled — and exercisers frustrated — by the general ineffectiveness of exercise as a weight-loss strategy. According to multiple studies and anecdotes, most people who start exercising do not lose as much weight as would be expected, given their increased energy expenditure. Some people add pounds despite burning hundreds of calories during workouts. Past studies of this phenomenon have found that exercise can increase the body’s production of appetite hormones, making some people feel ravenous after even a light workout and prone to consume more calories than they expended. But that finding, while intriguing, doesn’t fully explain the wide variability in people’s post-exercise eating habits. So, for the new study, published in the journal Marketing Letters, French and American researchers turned to psychology and the possible effect that calling exercise by any other name might have on people’s subsequent diets. In that pursuit, the researchers first recruited 56 healthy, adult women, the majority of them overweight. The women were given maps detailing the same one-mile outdoor course and told that they would spend the next half-hour walking there, with lunch to follow. Half of the women were told that their walk was meant to be exercise, and they were encouraged to view it as such, monitoring their exertion throughout. The other women were told that their 30-minute outing would be a walk purely for pleasure; they would be listening to music through headphones and rating the sound quality, but mostly the researchers wanted them to enjoy themselves. When the women returned from walking, the researchers asked each to estimate her mileage, mood and calorie expenditure. © 2014 The New York Times Company

Keyword: Obesity; Emotions
Link ID: 19691 - Posted: 06.04.2014

by Catherine de Lange Could your ideal diet be written in your genes? That's the promise of nutrigenomics, which looks for genetic differences in the way people's bodies process food so that diets can be tailored accordingly. The field had a rocky start after companies overhyped its potential, but with advances in genetic sequencing, and a slew of new studies, the concept is in for a reboot. Last week, Nicola Pirastu at the University of Trieste, Italy, and his colleagues told the European Society of Human Genetics meeting in Milan that diets tailored to genes that are related to metabolism can help people lose weight. The team used the results of a genetic test to design specific diets for 100 obese people that also provided them with 600 fewer calories than usual. A control group was placed on a 600-calorie deficit, untailored diet. After two years, both groups had lost weight, but those in the nutrigenetic group lost 33 per cent more. They also took only a year to lose as much weight as the group on the untailored diet lost in two years. If this is shown to work in bigger, randomised trials, it would be fantastic, says Ana Valdes, a genetic epidemiologist at the University of Nottingham, UK. Some preliminary information will soon be available from Europe's Food4Me project. It is a study of 1200 people across several countries who were given either standard nutrition advice, or a similarly genetically tailored diet. "It's testing whether we can get bigger changes in diet using a personalised approach, and part of that is using genetic information," says team member John Mathers, director of the Human Nutrition Research Centre at Newcastle University, UK. © Copyright Reed Business Information Ltd.

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 19690 - Posted: 06.04.2014

Joy Jernigan TODAY contributor Depression is a serious medical condition that affects millions of Americans — and nearly twice as many women as men. Symptoms can include persistent feelings of sadness or hopelessness and loss of interest in activities that were once pleasurable, according to the National Institute of Mental Health. Other symptoms include feelings of guilt or worthlessness, irritability, changes in appetite, increased fatigue, difficulty concentrating — even recurrent thoughts of suicide. About 12 million American women suffer from depression each year, women like Debi Lee. Although depression is treatable, most commonly with medications or counseling, many never seek help, often because they are too embarrassed or ashamed. "Depression is really a physical illness," said Dr. Andrew Leuchter, a psychiatrist at the Semel Institute for Neuroscience and Human Behavior at University of California, Los Angeles. It's a disorder that even can be seen in brain scans, with images clearly showing the difference between a normal functioning brain and the brain of someone suffering from depression. "When you show this image to a person who's struggling with depression and you show them that their brain looks different than the quote so-called healthy person, what's their reaction?" Shriver asked. "It's commonly one of relief," Leuchter said. Now, Dr. Leuchter says there's an innovative new treatment called synchronized transcranial magnetic stimulation, or sTMS, that may have the potential to provide relief. Dr. Leuchter, a consultant and stockholder in the company behind sTMS, says it syncs to each patient's brain, then stimulates it with low levels of magnetic energy, 30 minutes a day for several weeks.

Keyword: Depression
Link ID: 19689 - Posted: 06.04.2014

Ewen Callaway By controlling rats' brain cells they had genetically engineered to respond to light, researchers were able to create fearful memories of events that never happened — and then to erase those memories again. Neuroscientists can breathe a collective sigh of relief. Experiments have confirmed a long-standing theory for how memories are made and stored in the brain. Researchers have created and erased frightening associations in rats' brains using light, providing the most direct demonstration yet that the strengthening and weakening of connections between neurons is the basis for memory. “This is the best evidence so far available, period,” says Eric Kandel, a neuroscientist at Columbia University in New York. Kandel, who shared the 2000 Nobel Prize in Physiology or Medicine for his work unravelling the molecular basis of memory, was not involved in the latest study, which was published online in Nature1 on 1 June. In the 1960s and 1970s, researchers in Norway noticed a peculiar property of brain cells. Repeatedly delivering a burst of electricity to a neuron in an area of the brain known as the hippocampus seemed to boost the cell’s ability to talk to a neighbouring neuron. These communiqués occur across tiny gaps called synapses, which neurons can form with thousands of other nerve cells. The process was called long-term potentiation (LTP), and neuroscientists suspected that it was the physical basis of memory. The hippocampus, they realized, was important for forming long-term memories, and the long-lasting nature of LTP hinted that information might be stored in a neural circuit for later recall. © 2014 Nature Publishing Group,

Keyword: Learning & Memory; Emotions
Link ID: 19688 - Posted: 06.03.2014

Ian Sample, science correspondent Research on children in Denmark has found that boys with autism were more likely to have been exposed to higher levels of hormones in their mother's wombs than those who developed normally. Boys diagnosed with autism and related disorders had, on average, raised levels of testosterone, cortisol and other hormones in the womb, according to analyses of amniotic fluid that was stored after their mothers had medical tests during pregnancy. The findings add to a growing body of evidence that the biological foundations of autism are laid down well before birth and involve factors that go beyond the child's genetic make-up. The results may help scientists to unravel some of the underlying causes of autism and explain why boys are four to five times more likely to be diagnosed with the condition, which affects around one percent of the population. Amniotic fluid surrounds babies in the womb and contains hormones and other substances that they have passed through their urine. The liquid is collected for testing when some women have an amniocentesis around four months into their pregnancy. Scientists in Cambridge and Copenhagen drew on Danish medical records and biobank material to find amniotic fluid samples from 128 boys who were later diagnosed with autism. Compared to a control group, the boys with autism and related conditions had higher levels of four "sex steroid" hormones that form a biological production line in the body that starts with progesterone and ends with testosterone. "In the womb, boys produce about twice as much testosterone as girls, but compared with typical boys, the autism group has even higher levels. It's a significant difference and may have a large effect on brain development," said Simon Baron-Cohen, director of the Autism Research Centre at Cambridge University. © 2014 Guardian News and Media Limited

Keyword: Autism; Hormones & Behavior
Link ID: 19687 - Posted: 06.03.2014

By MARK OPPENHEIMER When our young daughters first decided to play on top of our Honda minivan, parked in our driveway, my wife was worried. But to me, it seemed no less safe than chasing a ball that frequently ended up in the street. And they loved the height, the novelty, the danger. So I let them stay. They never fell. And with the summer weather here, playing on the car is once again keeping them occupied for hours. Now that I have read Paul Raeburn’s “Do Fathers Matter?,” I know that my comfort with more dangerous play — my willingness to let my daughters stand on top of a minivan — is a typically paternal trait. Dads roughhouse with children more, too. They also gain weight when their wives are pregnant and have an outsize effect on their children’s vocabulary. The presence of dads can delay daughters’ puberty. But older dads have more children with dwarfism and with Marfan syndrome. In Mr. Raeburn’s book, there is plenty of good news for dads, and plenty of bad. A zippy tour through the latest research on fathers’ distinctive, or predominant, contributions to their children’s lives, “Do Fathers Matter?” is filled with provocative studies of human dads — not to mention a lot of curious animal experiments. (You’ll learn about blackbirds’ vasectomies.) But above all, Mr. Raeburn shows how little we know about the role of fathers, and how preliminary his book is. Its end is really a beginning, a prospectus for further research. Mr. Raeburn writes that “as recently as a generation ago, in the 1970s, most psychologists” believed that “with regard to infants, especially, fathers were thought to have little or no role to play.” When it came to toddlers and older children, too, the great parenting theories of the 20th century placed fathers in the background. Freud famously exalted, or damned, the mother for her influence. John Bowlby’s attachment theory, which he developed beginning in the 1940s, focused on the mother or “mother-figure.” © 2014 The New York Times Company

Keyword: Sexual Behavior
Link ID: 19686 - Posted: 06.03.2014

|By Christie Nicholson Conventional wisdom once had it that each brain region is responsible for a specific task. And so we have the motor cortex for handling movements, and the visual cortex, for processing sight. And scientists thought that such regions remained fixed for those tasks beyond the age of three. But within the past decade researchers have realized that some brain regions can pinch hit for other regions, for example, after a damaging stroke. And now new research finds that the visual cortex is constantly doing double duty—it has a role in processing not just sight, but sound. When we hear [siren sound], we see a siren. In the study, scientists scanned the brains of blindfolded participants as the subjects listened to three sounds: [audio of birds, audio of traffic, audio of a talking crowd.] And the scientists could tell what specific sounds the subjects were hearing just by analyzing the brain activity in the visual cortex. [Petra Vetter, Fraser W. Smith and Lars Muckli, Decoding Sound and Imagery Content in Early Visual Cortex, in Current Biology] The next step is to determine why the visual cortex is horning in on the audio action. The researchers think the additional role conferred an evolutionary advantage: having a visual system primed by sound to see the source of that sound could have given humans an extra step in the race for survival. © 2014 Scientific American

Keyword: Vision; Hearing
Link ID: 19685 - Posted: 06.03.2014