by Douglas Fox THE MAN dangles on a cable hanging from an eight-storey-high tower. Suspended in a harness with his back to the ground, he sees only the face of the man above, who controls the winch that is lifting him to the top of the tower like a bundle of cargo. And then it happens. The cable suddenly unclips and he plummets towards the concrete below. Panic sets in, but he's been given an assignment and so, fighting his fear of death, he stares at the instrument strapped to his wrist, before falling into the sweet embrace of a safety net. A team of scientists will spend weeks studying the results. The experiment was extreme, certainly, but the neuroscientist behind the study, David Eagleman at Baylor College of Medicine in Houston, Texas, is no Dr Strangelove. When we look back at scary situations, they often seem to have occurred in slow motion. Eagleman wanted to know whether the brain's clock actually accelerates - making external events appear abnormally slow in comparison with the brain's workings - or whether the slo-mo is just an artefact of our memory. It's just one of many mysteries concerning how we experience time that we are only now beginning to crack. "Time," says Eagleman, "is much weirder than we think it is." By understanding the mechanisms of our brain's clock, Eagleman and others hope to learn ways of temporarily resetting its tick. This might improve our mental speed and reaction times. What's more, since time is crucial to our perception of causality, a faulty internal clock might also explain the delusions suffered by people with schizophrenia. © Copyright Reed Business Information Ltd

Keyword: Attention; Learning & Memory
Link ID: 13381 - Posted: 06.24.2010

By Gisela Telis If your ears are still ringing from that last Metallica concert, scientists can't help you--but they may have figured out what's going on in your head. A type of small neuron in the inner ear, it seems, may help process painfully loud sounds. The discovery solves a 70-year-old mystery about what these neurons do--and may deepen understanding of hearing loss and impairment. Humans and other mammals owe their hearing to a forest of hairlike cells in the inner ear. As sound waves move into the ear, the hair cells sway along, and their motion releases electrical and chemical signals that the brain interprets as sound. Two kinds of neurons transmit those signals. Type I is the standard: It makes up 90% to 95% of all neurons in the inner ear and tells the brain about a sound's frequency, volume, and timing--all the ingredients of hearing as we know it. The remaining 5% of the neurons are type II, which were first described in 1937 and are smaller and harder to study. In fact, just a single study has reported success in connecting a type II neuron to an electrode, which is the main method for studying hearing cells. Hearing researcher Paul Fuchs and his colleagues at the Johns Hopkins University School of Medicine in Baltimore, Maryland, came up with a different way to isolate the elusive neurons. Instead of trying to find them within an intact ear, they dissected the inner ears of rats. During a window of only a few hours before the tissue samples died, the researchers tracked down the type II neurons, hooked them up to electrodes, and recorded what they did in the presence of a chemical that provokes the same reaction as sound in hearing cells. © 2009 American Association for the Advancement of Science

Keyword: Hearing
Link ID: 13380 - Posted: 06.24.2010

By Laura Sanders CHICAGO — Junk food elicits addictive behavior in rats similar to the behaviors of rats addicted to heroin, a new study finds. Pleasure centers in the brains of rats addicted to high-fat, high-calorie diets became less responsive as the binging wore on, making the rats consume more and more food. The results, presented October 20 at the Society for Neuroscience’s annual meeting, may help explain the changes in the brain that lead people to overeat. “This is the most complete evidence to date that suggests obesity and drug addiction have common neurobiological underpinnings,” says study coauthor Paul Johnson of the Scripps Research Institute in Jupiter, Fla. To see how junk food affects the brain’s natural reward system — the network of nerve cells that release feel-good chemicals — Johnson started at the grocery store. He loaded up on typical Western fare, including Ho Hos, sausage, pound cake, bacon and cheesecake. Johnson fed rats either a standard diet of high-nutrient, low-calorie chow, or unlimited amounts of the palatable junk food. Rats that ate the junk food soon developed compulsive eating habits and became obese. “They’re taking in twice the amount of calories as the control rats,” says Johnson’s coauthor Paul Kenny, also of Scripps. Johnson and Kenny wanted to know if this overeating affected the pleasure centers of the rats’ brains, the regions responsible for drug addiction. The researchers used electrical stimulations to activate these reward centers and induce pleasure. Rats could control the amount of feel-good stimulation by running on a wheel — the more they ran, the more stimulation they got. The rats fed junk food ran more, indicating that they needed more brain stimulation to feel good. © Society for Science & the Public 2000 - 2009

Keyword: Obesity; Drug Abuse
Link ID: 13379 - Posted: 06.24.2010

By JANE E. BRODY If you have ever slept on an arm and awakened with a “dead” hand, or sat too long with your legs crossed and had your foot fall asleep, you have some inkling of what many people with peripheral neuropathy experience day in and day out, often with no relief in sight. And numbness and tingling are hardly the worst symptoms of this highly variable condition, which involves damage to one or more of the myriad nerves outside the brain and spinal cord. Effects may include disabling pain, stinging, swelling, burning, itching, muscle weakness, twitching, loss of sensation, hypersensitivity to touch, lack of coordination, difficulty breathing, digestive disorders, dizziness, impotence, incontinence, and even paralysis and death. I realize now that I had a mild, reversible bout of peripheral neuropathy several decades ago when a misplaced shot of morphine damaged a sensory nerve in my thigh. It took three years for the nerve to recover, and for much of that time I could not tolerate anything brushing against my leg. One of my sons, too, was afflicted when a nerve behind his knee was injured during a basketball game. He had no feeling or mobility in his foot for nine months, but after several years the nerve healed and he regained full use of his foot. And a good friend was nearly paralyzed, also temporarily, following a flu shot, by a far more serious form of peripheral neuropathy — an autoimmune affliction called Guillain-Barré syndrome, in which one’s own antibodies attack the myelin sheath that protects nerves throughout the body. Copyright 2009 The New York Times Company

Keyword: Neuroimmunology; Movement Disorders
Link ID: 13378 - Posted: 06.24.2010

By NICHOLAS BAKALAR The first time the words “amyotrophic lateral sclerosis” appeared in The New York Times was in 1876, in an advertisement for a medical text; the disease had first been described by a French doctor in 1869. The Times did not mention it again until Arthur Daley, a Pulitzer Prize-winning sports columnist, reported on Lou Gehrig’s diagnosis in June 1939. The end of Gehrig’s record streak of 2,130 straight games came on May 2, but the explanation in The Times the next day was that Gehrig had “recognized his competitive decline” and that his withdrawal from the lineup “does not necessarily mean the end of his playing career.” A column by John Kieran the same day expressed certainty that “with a little rest he should begin to feel his oats again,” that all he really needed was “a breathing spell.” On June 2, a 120-word article on the sports page reported that Gehrig would be examined at the Mayo Clinic. Yet on June 12, with no public report about the results of the examination, Gehrig was back in the lineup for three innings in an exhibition game against the Kansas City Blues, a Yankee farm club. Finally on June 22, Daley, quoting Dr. H. C. Habein of the Mayo Clinic, wrote that the Iron Horse had amyotrophic lateral sclerosis, the first mention of the illness in the newspaper in 63 years. An Associated Press release printed below the article quoted the editor of the Journal of the American Medical Association saying that A.L.S. was “a well-established scientific diagnosis of a condition in which there is a hardening of the tissues in the spinal column and a wasting of the muscles dependent upon it,” but although the doctor must have known the facts, he said nothing of a fatal prognosis. Copyright 2009 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 13377 - Posted: 06.24.2010

By TARA PARKER-POPE Dementia is often viewed as a disease of the mind, an illness that erases treasured memories but leaves the body intact. But dementia is a physical illness, too — a progressive, terminal disease that shuts down the body as it attacks the brain. Although the early stages can last for years, the life expectancy of a patient with advanced dementia is similar to that of a patient with advanced cancer. The lack of understanding about the physical toll of dementia means that many patients near the end of life are subjected to aggressive treatments that would never be considered with another terminal illness. People with advanced dementia are often given dialysis and put on ventilators; they may even get preventive care that cannot possibly help them, like colonoscopies and drugs for osteoporosis or high cholesterol. “You can go to an intensive-care unit in most places,” said Dr. Greg A. Sachs, chief of general internal medicine and geriatrics at Indiana University School of Medicine, “and you’ll find people with dementia getting very aggressive treatment.” The continued focus on treatment to prolong life often means that pain relief is inadequate, and symptoms like confusion and anxiety are worsened. A new study suggests that family members would be far less likely to subject their loved ones to such treatment if they had a better understanding of dementia as progressive, debilitating illness that ultimately shuts down the body after years of mental deterioration. Copyright 2009 The New York Times Company

Keyword: Alzheimers
Link ID: 13376 - Posted: 06.24.2010

By SEAN B. CARROLL I have long suspected that fish are smarter than we give them credit for. As a child, I had an aquarium with several pet goldfish. They certainly knew it was feeding time when my hand appeared over their tank, and they excitedly awaited their delicious fish flakes. They also exhibited a darker, disturbing behavior. Evidently, a safe life with abundant food was not fulfilling. From time to time, either sheer ennui or the long gray Toledo winter got to one of the fish and it ended its torment with a leap to my bedroom floor. Maybe my anthropomorphizing is a bit over the top. But, really, just how smart are fish? Can they learn? A 10-gallon tank with a plastic sunken pirate ship is certainly not the most stimulating habitat. But in the colorful, diverse and dangerous world of coral reefs, fish must be able to recognize not only food, but also to discriminate friends from foes, and mates from rivals, and to take the best action. In such a complex and dynamic environment, it would pay to be flexible and able to learn. A series of studies has recently revealed that reef fish are surprisingly adaptable. Freshly caught wild fish quickly learn new tasks and can learn to discriminate among colors, patterns and shapes, including those they have never encountered. These studies suggest that learning and interpreting new stimuli play important roles in the lives of reef fish. Copyright 2009 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 13375 - Posted: 06.24.2010

by Irving Kirsch ARE we too quick to prescribe psychotropic medication for emotional and behavioural problems? Take Alzheimer's disease. In an attempt to reduce their aggressive behaviour, up to 60 per cent of people with Alzheimer's in Europe and North America are prescribed antipsychotic medications such as Risperdal (risperidone) and Zyprexa (olanzapine). The estimated cost of these drugs is £80 million a year in the UK alone. People given antipsychotics are sedated and become less aggressive or agitated, but compared with placebo the benefits seem modest at best. In 2006, a 42-centre trial in the US found no significant differences between antipsychotic drugs and placebo after 12 weeks. Other trials showed some advantages of drugs over placebo, but these were "modest" (Cochrane Database of Systematic Reviews, DOI: 10.1002/14651858.CD003012.pub2). The risks, however, are large. According to the UK Medicines and Healthcare Products Regulatory Agency, the medication produces a threefold increase in the risk of stroke (www.bit.ly/NN8p0). The drugs also double the risk of dying over a three-year period, according to a study funded by the UK's Alzheimer's Research Trust (The Lancet, Neurology, vol 8, p 151). Last week, 10 dementia groups, including the trust, demanded the UK government publish a long-delayed review of the use of antipsychotic drugs in dementia. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Schizophrenia
Link ID: 13374 - Posted: 06.24.2010

AGREEING that the sports authorities were shabby, intrusive and untruthful in their handling of the case of Caster Semenya, the 18-year-old South African runner who won a gold medal in Berlin in August, is one thing. Deciding who is or is not a woman is another. On October 11th the International Association of Athletics Federations said it would try to settle this question for future games. They will need brainpower to match the muscles that they administer. Scientists reckon that at least 1.7% of people are born with one of several dozen possible intersexual conditions. A few are apparent from birth, some become visible only at puberty and many may never be identified. Instead of two X chromosomes, some women have three; others have two XXs and an extra Y, or one of many other variations. Men may have an extra X chromosome or two on top of their normal XY combination. Not every culture divides the sexes absolutely. North American tribal customs feature “two-spirit” people who combined male and female attributes (anthropologists call these “berdache”, from a French word for catamite). In South Asia hijras are considered neither male nor female. They may be intersex people or men who take on feminine identities, sometimes after castration. They often have horrid lives. Anne Tamar-Mattis of Advocates for Informed Choice, an American pressure group, says that though legal systems assume that male and female are indisputable categories, none defines them. A rare exception is in Australia, where a Human Rights Commission report in March 2009 recommended that adults should be allowed to register their sex as “unspecified” on documents such as passports. In February 2009 an Austrian court ruled that surgery was not a prerequisite for sex and name changes. Similarly, Germany’s Federal Supreme Court ruled in 2005 that regarding an operation as a precondition for a legally valid sex change was increasingly problematic. © The Economist Newspaper Limited 2009.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 13373 - Posted: 06.24.2010

By Amanda Gardner (HealthDay News) -- A new study finds no differences in blood mercury levels between children who are developing normally and those diagnosed with autism or autism spectrum disorders. The findings, appearing online Oct. 19 in the journal Environmental Health Perspectives, may quell some of the debate surrounding mercury and autism. The researchers did not, for instance, look at whether mercury might play a causal role in this group of developmental disorders. "This is an excellent study that has addressed a very important question for many families about the role of mercury [in autism]," said Dr. Patricia Manning-Courtney, medical director of The Kelly O'Leary Center for Autism Spectrum Disorders at Cincinnati Children's Hospital Medical Center. "It's a very clear study [in] that no differences in mercury were seen. Is it going to put the questions to rest? I think no. It's another important contribution to the large body of knowledge on this topic, but I think it will still be an area of great controversy." Previous studies have shown higher blood mercury levels in people with autism, but the results, along with the quality of the studies, have been inconsistent. One of the biggest controversies claims that vaccines containing the preservative thimerosal, which contains mercury, might cause autism. But thimerosal is no longer used routinely in children's vaccines and, earlier this year, a U.S. court ruled that there is no scientific evidence that childhood vaccines such as the measles-mumps-rubella vaccine caused autism in children of parents seeking compensation from a federal fund. Copyright © 2009 ScoutNews, LLC.

Keyword: Autism; Neurotoxins
Link ID: 13372 - Posted: 06.24.2010

by Greg Miller Did you know that an octopus brain has more than 50 lobes and about as many neurons (100 million) as a mouse's brain? And that's not counting the smaller brains in each arm and the tiny brains (okay, ganglia) devoted to each sucker? Neither did I, until I spent the morning visiting with Cliff Ragsdale and his postdoc Shuichi Shigeno at the University of Chicago. Ragsdale and Shigeno think octopuses may have much to teach us about brain evolution. In size and complexity the octopus brain rivals that of many vertebrate species. But it's put together much, much differently. "This is as far from the vertebrate design as we can get in a successful, living animal," Ragsdale says. That raises interesting questions about whether the neural circuits that control movement, memory and other functions in an octopus brain work the same way as do the analogous circuits in other animals. To investigate, Shigeno has been using molecular methods to examine the anatomy, neurochemistry and developmental genetics of the octopus brain. He presented some of his preliminary findings yesterday at the Society for Neuroscience meeting in Chicago, and I'll post a longer discussion of this work (and more cool photos) later this week over on our Origins blog. Stay tuned. © 2008 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 13371 - Posted: 06.24.2010

By Laura Sanders CHICAGO — A toned, buff bod isn’t the only thing a workout is good for. Exercise protects special brain cells in monkeys’ brains and improves motor function, a new study finds. The data, presented at a news briefing October 18 in Chicago at the Society for Neuroscience’s annual meeting, adds to a growing body of evidence that shows exercise is good for the brain, too. “This is sort of a quiet revolution that’s been occurring in neuroscience,” says Carl Cotman, a brain aging expert at the University of California, Irvine, “to realize that physical activity at a certain level impacts the brain in a really profound way.” In the new study, researchers led by Judy Cameron of the University of Pittsburgh trained six adult female rhesus monkeys to run on treadmills built for humans. Over a period of three months, monkeys either ran, jogged or sat on a treadmill for five hours each week. Monkeys that ran got their heart rates to about 80 percent of maximum, comparable to a human training program that would increase cardiovascular fitness. The jogging monkeys’ heart rates reached about 60 percent of maximum. After this training period, the researchers hit the right side of the monkeys’ brains with a neurotoxin called MPTP, designed to selectively kill neurons that produce the signaling chemical dopamine. These neurons, and the dopamine they produce, regulate movement, and are the very same ones that die in people with Parkinson’s disease. © Society for Science & the Public 2000 - 2009

Keyword: Parkinsons
Link ID: 13370 - Posted: 06.24.2010

By Henry L. Roediger and Bridgid Finn For years, many educators have championed “errorless learning," advising teachers (and students) to create study conditions that do not permit errors. For example, a classroom teacher might drill students repeatedly on the same multiplication problem, with very little delay between the first and second presentations of the problem, ensuring that the student gets the answer correct each time. The idea embedded in this approach is that if students make errors, they will learn the errors and be prevented (or slowed) in learning the correct information. But research by Nate Kornell, Matthew Hays and Robert Bjork at UCLA that recently appeared in the Journal of Experimental Psychology: Learning, Memory and Cognition reveals that this worry is misplaced. In fact, they found, learning becomes better if conditions are arranged so that students make errors. People remember things better, longer, if they are given very challenging tests on the material, tests at which they are bound to fail. In a series of experiments, they showed that if students make an unsuccessful attempt to retrieve information before receiving an answer, they remember the information better than in a control condition in which they simply study the information. Trying and failing to retrieve the answer is actually helpful to learning. It’s an idea that has obvious applications for education, but could be useful for anyone who is trying to learn new material of any kind. © 1996-2009 Scientific American Inc.

Keyword: Learning & Memory
Link ID: 13369 - Posted: 06.24.2010

by Greg Miller Before this afternoon's social issues roundtable, I blithely assumed that neuroscience is mostly a good thing for society. It's all about understanding emotions, memory and cognition--the things that make us who we are--and tackling scourges such as Alzheimer's disease and depression. So I was thrown a bit off-guard by the opening remarks of the session moderator, Alan Leshner. "I think when the rest of society finds out what the broader implications of neuroscience research are, they're not going to like it," Leshner said. The other speakers picked up this troubling thread and highlighted aspects of neuroscience research that have the potential to elicit unease in the general population. Philosopher Patricia Churchland of the University of California, San Diego, spoke about the implications of research on the neural mechanisms of decision-making (which tend to sound pretty deterministic) for the widely held view that people must be held responsible for their actions. Cognitive neuroscientist Barbara Sahakian of the University of Cambridge, U.K., cited recent evidence that the use of cognitive-enhancing drugs such as modafinil is increasing among teenagers, raising questions about long-term effects on the still-developing adolescent brain, among other ethical worries. And philosopher Jonathan Moreno of the University of Pennsylvania flew through a history of military uses and abuses of psychology and neuroscience research, ranging from 1950s work on using LSD to pry secrets from enemy spies to current interest in using the "trust hormone" oxytocin to loosen lips. © 2008 American Association for the Advancement of Science.

Keyword: Emotions; Learning & Memory
Link ID: 13368 - Posted: 06.24.2010

By Sam Kean Two medical problems caused by misfiring electrical signals, epilepsy and heart arrhythmia, probably have a common molecular cause, scientists report. The research points to treatments that could lower the chances of young people dying of seizures. The scientists, at Baylor College of Medicine in Houston, Texas, were studying mice that had a mutation in the KCNQ gene, which builds potassium ion channels that set up an action potential across a cell membrane. These channels help the heart beat by resetting the potential after cardiac muscle cells contract. The mutation--also found in humans--produces a faulty protein that delays restoration of the potential, causing erratic beating and sometimes death. The ion channel was long thought to operate only in heart muscle, but recent work implied that it functions in other tissues. Now Alica Goldman, a neurologist and co-author of the paper, has discovered the first definitive evidence that the channel was working in mouse neurons. It was especially active in regions of the brain susceptible to seizures, the researchers report online this week in Science Translational Medicine. The team also monitored the mutant mice with EEG and ECG machines and determined that seizures often accompanied abnormal heart rhythm. "This is exciting because it provides the first molecular clue" that potassium ion channels underlie epilepsy and arrhythmia, says Jeffrey Noebels, a neurologist and lead author of the paper. © 2009 American Association for the Advancement of Science.

Keyword: Epilepsy
Link ID: 13367 - Posted: 06.24.2010

By Carina Storrs Two decades ago, the discovery of neuropeptide Y (NPY), a peptide in the mammalian brain involved in food-seeking behavior, sparked a search for a weight-loss remedy that could interfere with its activity. Eventually the promise of other drug targets, along with the possible side effects of targeting NPY, put a damper on the effort—until now. New findings about the action of this appetite-promoting peptide could bring NPY back to the front burner. A study released this week in Cell reports on fruit fly neural circuitry that is affected by the drosophila equivalent of NPY—dNPF. The latter peptide disrupts a group of neurons that would normally put the brakes on tapping memory to search for food. Instead, dNPF allows neurons to release signals that prompt flies to hunt for a meal. By blocking the effect that dNPF has on neurons that interact with drosophila's memory center, the researchers found they could halt the flies' feeding frenzy, and trick them into thinking they were full, even though they had not eaten. The fact that NPY in mammals has similar appetite-inducing activity as its drosophila analogue suggests that it might also govern an as-yet unknown network in the human brain that regulates our desire to seek sustenance. "We know quite a lot about the memory system for olfactory memory in the fruit flies. That gave us some hope that we would be able to find a site of integration between [hunger] state and…memory," says Scott Waddell, an associate professor of neurobiology at the University of Massachusetts Medical School in Worcester, and supervisor of the new research. © 1996-2009 Scientific American Inc.

Keyword: Obesity
Link ID: 13366 - Posted: 06.24.2010

Annabel McGilvray, ABC Science Online -- Animal welfare researchers have uncovered why city-living domestic dogs may be prone to nuisance barking. In this month's issue of Australian Veterinary Journal, a team from the University of Queensland's Center for Animal Welfare and Ethics report a case-control survey of 150 dog owners including 72 dogs whose owners had sought treatment for nuisance barking. Barking can be classified as being a nuisance when it causes distress or interruption to the life of the dogs' owners or neighbors. The results suggest dogs most likely to become nuisance barkers are young dogs from herding breeds such as collies and kelpies, those bred in a home environment, have access to indoors or live with other dogs. Co-author of the report, Clive Phillips said the work was prompted by the high number of public complaints and inquiries about nuisance barking, with studies suggesting approximately a third of dog owners possess at least one nuisance barker. "We wanted to look at the factors relating to the dog, the owner and the environment that may increase the risk of nuisance barking." He said, barking may be caused by separation anxiety, perceived threats in the environment and sometimes to simple social interaction, canine-style. But human actions and responses also play a role. © 2009 Discovery Communications, LLC.

Keyword: Animal Communication; Stress
Link ID: 13365 - Posted: 06.24.2010

By Laura Sanders CHICAGO -- Magicians and neuroscientists may not seem like a likely match, but they have one important thing in common: A fascination with the brain. As Science News pointed out in this article about science and magic in April, neuroscientists delve deep into the human mind to see how things like attention, perception and memory work, while magicians manipulate these very same things to confound their audience. This unlikely alliance was solidified October 17 at the Society for Neuroscience’s Annual Meeting in Chicago as two world-class magicians demonstrated some of their tricks to an audience of thousands of neuroscientists. (The size of the scientist crowd may have rivaled the motley crew of America’s Got Talent hopefuls, who were waiting in a monster line that snaked around a different part of the conference center. Although neuroscientists seem like they might be a tough crowd, everyone in the room was enamored. By all reports, the scientists seemed thrilled to have such interesting new colleagues. Apollo Robbins, known professionally as the “Gentleman Thief,” has an unusual set of skills that allowed him to, among other dastardly deeds, “borrow” Jennifer Garner’s engagement ring, switch Troy Aikman and Jerome Bettis’ licenses, and relieve Jimmy Carter’s secret service agents of their wallets, watches and confidential itineraries. (For more of Robbins’ rap sheet, check out his website Istealstuff.com © Society for Science & the Public 2000 - 2009

Keyword: Attention; Vision
Link ID: 13364 - Posted: 06.24.2010

By Melinda Wenner We smile because we are happy, and we frown because we are sad. But does the causal arrow point in the other direction, too? A spate of recent studies of botox recipients and others suggests that our emotions are reinforced—perhaps even driven—by their corresponding facial expressions. Charles Darwin first posed the idea that emotional responses influence our feelings in 1872. “The free expression by outward signs of an emotion intensi­fies it,” he wrote. The esteemed 19th-cen­tury psychologist William James went so far as to assert that if a person does not express an emotion, he has not felt it at all. Although few scientists would agree with such a statement today, there is evidence that emotions in­volve more than just the brain. The face, in particular, appears to play a big role. This February psychologists at the University of Cardiff in Wales found that people whose ability to frown is comp­romised by cosmetic botox inject­ions are happier, on average, than people who can frown. The researchers administered an anxiety and depression questionnaire to 25 females, half of whom had received frown-inhibiting botox injections. The botox recipients reported feeling happier and less anxious in general; more important, they did not report feeling any more attractive, which suggests that the emotional effects were not driven by a psychological boost that could come from the treatment’s cosmetic nature.

Keyword: Emotions
Link ID: 13363 - Posted: 06.24.2010

By Carina Storrs Seeing is believing when it comes to emotions. We smile, we gasp, we yawn when we see others do the same—a phenomenon called emotional contagion. A new study published last week in Proceedings of the National Academy of Sciences finds that emotional contagion occurs even if the "seeing" step is bypassed. The blind patients in the study could not consciously see images of the faces of happy or fearful people that they were shown. Although their eyes and optic nerves were functional, the region of their brains involved in visual processing had been damaged. Instead, other parts of the brain took over, allowing the subjects to still respond normally with their own happy or scared facial expressions. These patients also made the appropriate happy or fearful face in response to emotions that were communicated through bodily expressions, suggesting that blind empathy can happen even without a facial template to imitate. "We're actually infected by the emotions of others. [This study shows] this phenomenon can be carried out in the absence of visual awareness," says Marco Tamietto, a neuroscience researcher at Tilburg University in the Netherlands and lead author of the study. "We can say that emotional contagion cannot be reduced to a simple mimicry." To tease apart the mechanism underlying emotional contagion, Tamietto and his colleagues took advantage of what is known in neuroscience as "blindsight". Starting a few decades ago, researchers found that patients who have damage to the part of the brain called the visual cortex, which processes visual information, retain a sort of sixth sense of sight.

Keyword: Vision; Emotions
Link ID: 13362 - Posted: 06.24.2010