David Cyranoski More than a decade of research hinting that magnesium supplements might boost your brain power is finally being put to the test in a small clinical trial. The research, led by biopharmaceutical company Magceutics of Hayward, California, began testing the ability of its product Magtein to boost magnesium ion (Mg2+) levels in the brain earlier this month. The trial will track whether the ions can decrease anxiety and improve sleep quality, as well as following changes in the memory and cognitive ability of participants. But critics caution that the trial in just 50 people is too small to draw definitive conclusions. Neuroscientist Guosong Liu of the Massachusetts Institute of Technology in Cambridge, who founded Magceutics, plans eventually to test whether Magtein can be used to treat a wider range of conditions, including attention deficit hyperactivity disorder (ADHD) and Alzheimer’s disease. But Liu knows that it will be difficult to convince other scientists that something as simple as a magnesium supplement can have such profound effects. It is almost “too good to be true”, he says. Many scientists contacted by Nature agreed with that sentiment. One clinical researcher cautioned against “over-excitement about a magic drug for a major disorder”. And others wonder whether the study will even be able to prove anything conclusively. “I am very sceptical that the proposed trial will provide the answer to the question being tested,” says Stephen Ferguson, a biochemist at the University of Western Ontario in London, Ontario. © 2012 Nature Publishing Group

Keyword: Learning & Memory; Sleep
Link ID: 17430 - Posted: 10.27.2012

By Katherine Harmon With a juicy insect dinner perched on a leaf above the water, what is a hungry little archer fish down below to do? Knock it down with a super-powered, super-precise jet of water that packs six times the power the fish could generate with its own muscles, according to new findings published online October 24 in PLoS ONE. The stunning spitting power of the amazing archer fish (Toxotes jaculatrix) was first described in the 18th century. The creature lives in mostly in mangrove forests and estuaries where insects are prevalent—above water, that is. And these tasty treats are not easily knocked off of the plants that hang over the archer fish’s territory. The insects, such as grasshoppers, can hang on with a force some 10 times their own body weight. So the archer fish has developed an impressive strategy for fetching food that not many other fish can reach. Its water jet can target and dislodge a single insect so that it falls into the water for the fish to eat. Just how the fish manages to do this—and in less than a second—had remained a mystery. Many scientists figured that the source must be a special organ in the fish’s body. “The origin of the effectiveness of the jet squirted by the archer fish has been searched for inside of the fish for nearly 250 years,” Alberto Vailati, a physicist at the University of Milan and co-author of the new paper, said in a prepared statement. © 2012 Scientific American

Keyword: Biomechanics; Vision
Link ID: 17429 - Posted: 10.27.2012

With bright blue hair and tattoos, Dr Caspar Addyman is not your average scientist. But then Britain's "Babylab" is not your average laboratory. Here, inside one of the world's leading infant-research units, Dr Addyman has spent the morning filtering through the results of his new Baby Laughter project. It is the first in-depth study since the Sixties into what makes infants chuckle. Last time around, the experiment involved a toy clown attached to a piece of string, which scientists held in front of their tiny, unwitting human guinea pigs to see if and when they would laugh. Fortunately Dr Addyman's experiment, which he launched in August this year, is a little more complex. "Smiling and laughing are indices of our understanding of the world. Adults laugh at something when they find it surprising or unusual; it is exactly the same for babies," he explains. "Finding out what makes infants laugh teaches us more generally about how humans understand and respond to the world around them, and also the ways in which that can change." His gleeful subjects, who are all aged between two months and two years, are helping him to hunt for information that could eventually be used to determine how different developmental groups – for instance, people with autism or Down syndrome – respond to stimuli at different stages, which might ultimately lead to interventions. It is all smiles in Babylab HQ, at the Centre for Brain and Cognitive Development, Birkbeck, University of London. The lab was responsible earlier this year for a breakthrough study in autism which demonstrated a difference in brainwave patterns in infancy between children who later went on to develop the condition and those who did not. © independent.co.uk

Keyword: Emotions; Development of the Brain
Link ID: 17428 - Posted: 10.27.2012

By ANAHAD O'CONNOR Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Physical exercise not only protected against such age-related brain changes, but also had more of an effect than mentally and socially stimulating activities. In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities. Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the brain’s white matter, which is considered the “wiring” of the brain’s communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and I.Q. As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study and a senior research fellow at Edinburgh. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.” Copyright 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 17427 - Posted: 10.27.2012

Smoking cigarettes throughout adulthood reduces life expectancy by about 11 years in women but quitting avoids much of the extra risk, a new large study shows. The Million Women Study in the UK recruited 1.3 million British women who were born in the early 1940s to look at the hazards of smoking and the benefits of stopping at various ages. Women in North America took up smoking decades later than men. Women in North America took up smoking decades later than men. (Jonathan Alcorn/Reuters) In most of Europe, Canada and the U.S., the popularity of smoking among young women reached its peak in the 1960s, decades later than for men. Among women in the study who smoked cigarettes through their adult lives, the mortality rate was three times that of women who never smoked or who stopped well before middle age, Sir Richard Peto of the University of Oxford and his co-authors said in Saturday's issue of the journal Lancet. "Stopping before 40 years of age, and preferably well before, avoids more than 90 per cent of this excess mortality; stopping before 30 years of age avoids more than 97 per cent of it," the study's authors concluded. "This does not, however, mean that it is safe to smoke until 40 years and then stop, for women who do so have throughout the next few decades a mortality rate 1.2 times that of never-smokers." Study participants were recruited from 1996 to 2001. They filled in questionnaires about the lifestyle, medical and social factors and were resurveyed by mail three and eight years later. © CBC 2012

Keyword: Drug Abuse
Link ID: 17426 - Posted: 10.27.2012

By Laura Sanders Anesthesiologists aren’t totally lying when they say they’re going to put you to sleep. Some anesthetics directly tap into sleep-promoting neurons in the brain, a study in mice reveals. The results may help clarify how drugs that have been used around the world for decades actually put someone under. “It’s kind of shocking that after 170 years, we still don’t understand why they work,” says study coauthor Max Kelz of the University of Pennsylvania in Philadelphia. Most neurons in the brain appear to be calmed by anesthetics, says neuropharmacologist and anesthesiologist Hugh Hemmings Jr. of Weill Cornell Medical College in New York City. But the new results, published online October 25 in Current Biology, show that two common anesthetics actually stimulate sleep-inducing neurons. “It’s unusual for neurons to be excited by anesthetics,” Hemmings says. In the study, Kelz, Jason Moore, also of the University of Pennsylvania, and colleagues studied the effects of the anesthetics isoflurane and halothane. Mice given the drugs soon became sleepy, as expected. Along with this drowsiness came a jump in nerve cell activity in a part of the brain’s hypothalamus called the ventrolateral preoptic nucleus, or VLPO. Not all neurons in the VLPO are the same. Some are involved in kicking off sleep, while neighboring neurons don’t seem to play a role. The anesthetics affected only the VLPO neurons that promote sleep, Moore and his colleagues found. © Society for Science & the Public 2000 - 2012

Keyword: Sleep
Link ID: 17425 - Posted: 10.27.2012

By Daisy Yuhas We're all familiar with the feeling—waking up from a restless night only to realize that this will be a very long, sleepy day. Recent research reveals that honeybees are also sensitive to sleep deprivation, and although a cup of coffee may give you a morning buzz, the bees aren't so lucky. Neurobiologists at the Free University of Berlin have found that sleepy bees fail to remember lessons learned the day before, a finding that could help scientists discover the neural processes involved in sleep and memory formation. They present their research October 25 in the Journal of Experimental Biology. "We started with the idea that we could look for a neural substrate of learning and memory in bees, since they have a wonderful memory, can be easily trained, and we know their brain well at the neuronal level," says study co-author Randolf Menzel. After characterizing how honeybees find their way home when released in a new location, the scientists captured and then released bees in unfamiliar territory some 600 meters from their hive. In addition to tracking how long the bees needed to return home, the researchers monitored bee sleep. Bees take brief naps throughout the day in addition to longer periods of nocturnal sleep. (Snoozing bees are easy to spot because their antennae droop.) The scientists made their observations both by watching bees in person and by tracking their activity via radio-frequency devices that they glued onto some of the insects. © 2012 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 17424 - Posted: 10.27.2012

By Michael Balter “What would you do with a brain if you had one?” Dorothy’s question to the Scarecrow in The Wizard of Oz elicited one of the movie’s most delightful songs, in which her straw-filled friend assured her that, among other things, he could “think of things I’d never thunk before.” But the Scarecrow seemed to do quite well without one, thus avoiding the high energy costs of fueling and cooling a human brain—which, with an average volume of about 1,400 cubic centimeters, is humongous relative to our body size. How did our brains get so big? Researchers have put forward a number of possible explanations over the years, but the one with the most staying power is an idea known as the social brain hypothesis. Its chief proponent, psychologist Robin Dunbar of Oxford University, has argued for the past two decades that the evolution of the human brain was driven by our increasingly complex social relationships. We required greater neural processing power so that we could keep track of who was doing what to whom. Our expanded brains could have been practical for other things, of course, such as innovations in tool use and food gathering. Most researchers, including Dunbar, agree that these hypotheses are not mutually exclusive. Whatever the reasons for the very large human noggin, there is a lot of explaining to do, because big brains have a lot going against them. The oversized Homo sapiens brain let us take over the planet, build cities, send space probes to Mars, and do all the other marvelous things that we humans are so proud of. But none of these things makes us much better at reproducing, and in terms of evolution, that’s really all that matters. © 2012 The Slate Group, LLC.

Keyword: Evolution; Development of the Brain
Link ID: 17423 - Posted: 10.26.2012

by Sara Reardon Sleeping helps us reset our brains and calm our emotions. Perhaps it can do more, though: if sleepers are exposed to odours they associate with bad memories, it appears they can lose the fear those memories bring. Previous studies have shown that sleep helps eliminate fear in general. But whether it is possible to focus this effect through the careful use of odours has not been tested in humans. Katherina Hauner and Jay Gottfried of Northwestern University in Evanston, Illinois, exposed subjects to four pictures of faces and a series of inoffensive smells such as mint. When one of the faces appeared, the volunteers got a painful electric shock. Afterwards, the researchers measured the amount of electricity conducted by the subjects' skin – a measure that goes up when afraid, because the sweat produced is a good conductor. The researchers found that conductance spiked whenever the volunteers saw the face associated with the shock. They then let half the subjects sleep, and exposed this group to variable amounts of the odour that had been presented along with the "painful" face. The next day, these volunteers were much less afraid of the face – and those with the least fear were those that had received the highest exposure to the odour while asleep. Brain scans also showed that brain areas associated with fear and with memory were less active after this exposure. © Copyright Reed Business Information Ltd.

Keyword: Sleep; Learning & Memory
Link ID: 17422 - Posted: 10.25.2012

Lizzie Buchen A popular political advertisement from early this summer begins with US President Barack Obama addressing a crowd of moon-eyed supporters. Suddenly, the screen goes dark to a crescendo of minor chords. Phrases such as “Fear and Loathing”, “Nauseating” and “Divide and Conquer” flash onto the screen, along with video clips of commentators complaining that Obama has used scare tactics to manipulate voters. In the final scene, the iconic poster from Obama's 2008 election campaign appears, the word HOPE transforming into FEAR as it bursts into flames. The advertisement, produced by the conservative organization American Crossroads in Washington DC, is typical of those that have come to dominate the US airwaves and YouTube in preparation for next month's presidential election. Emerging from both the right and the left, these commercials increasingly resemble horror films as they seek to sway voters by triggering basic emotions such as fear, anger and disgust. That strategy fits with emerging scientific evidence about how people acquire their political beliefs. In the past, political scientists agreed that social forces — most importantly, parents and the childhood environment — strongly influenced whether people became conservative or liberal, and whether they voted or engaged in politics at all. “We now know that it is probably not the whole story,” says John Jost, a psychologist at New York University. An increasing number of studies suggest that biology can exert a significant influence on political beliefs and behaviours. Biological factors including genes, hormone levels and neurotransmitter systems may partly shape people's attitudes on political issues such as welfare, immigration, same-sex marriage and war. And shrewd politicians might be able to take advantage of those biological levers through clever advertisements aimed at voters' primal emotions. © 2012 Nature Publishing Group

Keyword: Emotions; Genes & Behavior
Link ID: 17421 - Posted: 10.25.2012

by Helen Thomson Paralysis may no longer mean life in a wheelchair. A man who is paralysed from the trunk down has recovered the ability to stand and move his legs unaided thanks to training with an electrical implant. Andrew Meas of Louisville, Kentucky, says it has changed his life (see "I suddenly noticed I can move my pinkie", below). The stimulus provided by the implant is thought to have either strengthened persistent "silent" connections across his damaged spinal cord or even created new ones, allowing him to move even when the implant is switched off. The results are potentially revolutionary, as they indicate that the spinal cord is able to recover its function years after becoming damaged. Previous studies in animals with lower limb paralysis have shown that continuous electrical stimulation of the spinal cord below the area of damage allows an animal to stand and perform locomotion-like movements. That's because the stimulation allows information about proprioception – the perception of body position and muscle effort – to be received from the lower limbs by the spinal cord. The spinal cord, in turn, allows lower limb muscles to react and support the body without any information being received from the brain (Journal of Neuroscience, doi.org/czq67d). Last year, Susan Harkema and Claudia Angeli at the Frazier Rehab Institute and University of Louisville in Kentucky and colleagues tested what had been learned on animals in a man who was paralysed after being hit by a car in 2006. He was diagnosed with a "motor complete" spinal lesion in his neck, which means that no motor activity can be recorded below the lesion. © Copyright Reed Business Information Ltd

Keyword: Regeneration
Link ID: 17420 - Posted: 10.25.2012

By Katherine Harmon Getting seven to eight solid hours of sleep each night might seem an almost impossible luxury to many people. But not getting enough sleep is known to impair mental function and increase the risk for heart disease, among other ill effects. Accumulating evidence also suggests that even short-term, partial sleep deprivation could pave the way for weight gain and other negative metabolic consequences. More than 28 percent of adults in the U.S. report that they get less than six hours of sleep a night, with this cumulative deprivation becoming more common in the past three decades. And now that more than 35 percent of U.S. adults are currently obese, researchers have been searching for potential links between the two conditions, in hopes of reducing the increasing health and economic burden of obesity. Establishing lack of sleep as a risk factor for weight gain could have important clinical and public health effects, possibly allowing people to make simple lifestyle changes to improve their metabolic health. A new report, published online October 24 in the Journal of the Academy of Nutrition and Dietetics, reviews 18 carefully controlled laboratory studies that tested human subjects' physiological and behavioral responses to sleep deprivation as they relate to metabolic health. Reena Mehra, an associate professor of medicine who studies sleep and health at Case Western Reserve University School of Medicine and who was not involved in the new analysis, notes that the new paper is "a well done review of the experimental data." © 2012 Scientific American

Keyword: Obesity; Sleep
Link ID: 17419 - Posted: 10.25.2012

By Rachel Ehrenberg Chimps, gibbons and other primates are not just humans’ evolutionary cousins; a new analysis suggests they are also our blood brothers. The A, B and O blood types in people evolved at least 20 million years ago in a common ancestor of humans and other primates, new research suggests. The analysis deepens a mystery surrounding the evolutionary history of the ABO blood system, and should prompt further research into why the different blood groups have persisted over time, Laure Ségurel of the University of Chicago and colleagues report online October 22 in the Proceedings of the National Academy of Sciences. “Their evidence is rather convincing that this is a shared, very old capability that has remained throughout the divergence of the species,” says doctor and transfusion specialist Martin Olsson of Lund University in Sweden. Different forms of a single blood type gene determine what types of molecules sit on your red blood cells: type A molecules, type B molecules, A and B together, or no intact surface molecules in the case of type O (O was originally called type C, then was changed to O for the German “ohne,” meaning “without”). The A, B and O versions of the gene differ only slightly, and scientists have debated two scenarios to explain their evolution. One posits that the A version of the gene existed long ago, and the B and/or O versions later cropped up independently in several species (including humans, gorillas, baboons and chimps). Alternatively, all of those species may have inherited the A and B types from a single ancestor. © Society for Science & the Public 2000 - 2012

Keyword: Evolution
Link ID: 17418 - Posted: 10.25.2012

By Ferris Jabr Scientists have mapped, charted, modeled and visualized the human brain in many different ways. They have marked the boundaries of the organ’s four major lobes: the frontal, parietal, temporal and occipital lobes. They have divvied up the cortex into more than 50 Broadmann areas—small regions characterized by particular cell types and specific cognitive functions, such as processing speech and recognizing faces. Researchers have tagged individual neurons with fluorescent proteins, transforming gray tissue into stunning brainbows, and followed water molecules as they move through the nervous system to trace ribbons of neural tissue linking one brain region to another. More recently, some scientists have championed the importance of connectomes—detailed wiring diagrams of all the connections between neurons in a given nervous system or brain. Thoroughly understanding the brain, proponents of connectomics argue, requires precise maps of its neural circuits. The standard way of making a connectome is serial electron microscopy—chopping up an animal’s brain into thin sheets, taking photos of all the resident neurons through an electron microscope and using those photos to painstakingly reconstruct the connections between neurons. In the 1970s biologist Sydney Brenner and his colleagues began using this technique to map the 302 neurons and 7,000 neural connections, or synapses, in the nervous system of a tiny worm known as Caenorhabditis elegans. It took them more than 12 years to finish the map. So far, C. elegans is the only animal with such a thorough connectome. Since mammalian brains contain millions or billions of neurons and billions or trillions of synapses, depending on the species, researchers are searching for faster and cheaper ways to create connectomes. At Harvard University, for example, Jeff Lichtman and his colleagues have constructed an Automatic Tape-Collecting Lathe Ultramicrotome (ATLUM)—a machine that speeds up the business of slicing up brain tissue into thin sheets with conveyor-belt efficiency. © 2012 Scientific American

Keyword: Brain imaging
Link ID: 17417 - Posted: 10.24.2012

Why some people respond to treatments that have no active ingredients in them may be down to their genes, a study in the journal PLoS ONE suggests. The so-called "placebo effect" was examined in 104 patients with irritable bowel syndrome (IBS) in the US. Those with a particular version of the COMT gene saw an improvement in their health after placebo acupuncture. The scientists warn that while they hope their findings will be seen in other conditions, more work is needed. Edzard Ernst, a professor of complementary medicine at the University of Exeter, said: "This is a fascinating but very preliminary result. "It could solve the age-old question of why some individuals respond to placebo, while others do not. "And if so, it could impact importantly on clinical practice. "But we should be cautious - the study was small, we need independent replications, and we need to know whether the phenomenon applies just to IBS or to all diseases." Gene variants The placebo effect is when a patient experiences an improvement in their condition while undergoing an inert treatment such as taking a sugar pill or, in this case, placebo acupuncture, where the patient believes they are receiving acupuncture but a sham device prevents the needles going into their body. BBC © 2012

Keyword: Pain & Touch; Genes & Behavior
Link ID: 17416 - Posted: 10.24.2012

by Joel Winston Never mind the bitter end – it is the bitter beginning of an infection that triggers an immune response. We know that taste receptors on the tongue can detect bitter foods, but it turns out that there are also identical taste receptors in the upper airway. Noam Cohen at the University of Pennsylvania in Philadelphia and his team think they know why. They grew cell cultures from sinus tissue samples collected from surgical patients, and found that bitter taste receptors in the tissue picked up the presence of Pseudomonas aeruginosa, a bacterium that can cause pneumonia. The sinus tissue responded by producing nitric oxide to kill the invading microbes. "Certain people have strong innate defences against these bacteria, which is based on their ability to detect bitterness," says Cohen. "Others who don't really 'taste' these bitter compounds have a weakened defence." The research could lead to nasal sprays designed to activate the taste receptors and boost people's natural defences against sinus infections. "This is probably the most exciting clinical link found for bitter receptors," says Liquan Huang of the Monell Chemical Senses Center in Philadelphia, Pennsylvania, who was not involved in the study. "However, further work is needed to see if this can be translated into treatments." Journal reference: Journal of Clinical Investigation, doi.org/jj4 © Copyright Reed Business Information Ltd.

Keyword: Chemical Senses (Smell & Taste); Neuroimmunology
Link ID: 17415 - Posted: 10.24.2012

by Elizabeth Norton The ability to recognize faces is so important in humans that the brain appears to have an area solely devoted to the task: the fusiform gyrus. Brain imaging studies consistently find that this region of the temporal lobe becomes active when people look at faces. Skeptics have countered, however, that these studies show only a correlation, but not proof, that activity in this area is essential for face recognition. Now, thanks to the willingness of an intrepid patient, a new study provides the first cause-and-effect evidence that neurons in this area help humans recognize faces—and only faces, not other body parts or objects. An unusual collaboration between researchers and an epilepsy patient led to the discovery. Ron Blackwell, an engineer in Santa Clara, California, came to Stanford University in Palo Alto, California, in 2011 seeking better treatment for his epilepsy. He had suffered seizures since he was a teenager, and at age 47, his medication was becoming less effective. Stanford neurologist Josef Parvizi suggested some tests to locate the source of the seizures—and also suggested that it might be possible to eliminate the seizures by surgically destroying a tiny area of brain tissue where they occurred. Parvizi used electrodes placed on Blackwell's scalp to trace the seizures to the temporal lobe, about an inch above Blackwell's right ear. Then, surgeons placed more electrodes on the surface of Blackwell's brain, near the suspect point of origin in the temporal lobe. Parvizi stimulated each electrode in turn with a mild current, trying to trigger Blackwell's seizure symptoms under safe conditions. "If we get those symptoms, we know that we are tickling the seizure node," he explains. © 2010 American Association for the Advancement of Science.

Keyword: Attention
Link ID: 17414 - Posted: 10.24.2012

by Shaoni Bhattacharya Talk about having your cake and eating it. Fasting might not be the only route to a longer life – a hormone seems to work just as well, for mice at least. We know that some animals can extend their lifespan by consuming fewer calories. Engineered mice can get the same effect by simply pumping out high levels of a hormone normally produced during a fast, according to Steven Kliewer and David Mangelsdorf at the University of Texas Southwestern Medical Center in Dallas. Their team found that mice engineered to make higher levels of the hormone, FGF21, increased their lifespan on average by over a third. "What we are seeing is the benefit of caloric restriction without having to diet," he says. Humans have the hormone too, and Kliewer believes FGF21 has the potential to extend the human "health-span" – the time we live healthy lives. The researchers believe FGF21 may act to prolong life by affecting pathways such as the insulin-like growth factor-1 (IGF-1) pathway implicated in ageing. "It blocks growth hormones promoting pathways which are associated with diseases, including cancers and metabolic diseases, and as a consequence these animals live longer," says Kliewer. © Copyright Reed Business Information Ltd.

Keyword: Obesity; Hormones & Behavior
Link ID: 17413 - Posted: 10.24.2012

By Maggie Fox and Linda Carroll Does this sound like you? Two cups of coffee in the morning, a coffee break at 11 or so, another cup in the afternoon and a cup after dinner? That might be enough to interfere with sleep or even give some people the jitters, but it’s nowhere near an overdose. It may also be nothing compared to what some teenagers are consuming to deal with schoolwork or job pressures. James Stone, a 19-year-old from Wallingford, Conn., died in 2006 after he took nearly two dozen NoDoz tablets. Each tablet has about 200 mg of caffeine – about twice that found in a cup of coffee. But while it would be near impossible to down 48 cups of coffee in a few hours, it’s relatively easy to pop a handful of small tablets. Now the question is whether guzzling energy drinks might be as dangerous as popping No-Doz. The Food and Drug Administration is investigating reports that five people died and one survived a heart attack after consuming energy drinks. It is not yet clear whether the drinks actually caused – or even contributed to - those adverse events, said FDA spokeswoman Shelly Burgess. “So far there’s been no causal link,” Burgess said. “There could have been other products involved. We don’t know that yet and that’s why we’re taking this seriously and looking into it.” © 2012 NBCNews.com

Keyword: Drug Abuse
Link ID: 17412 - Posted: 10.24.2012

By Scicurious Picture this: the prince has won his way past the dragon, past the huge walls of briars. He paces slowly through the sleeping castle, toward the tower where the princess lies, in a deep, deep sleep. Finally he sees her, leans over her lovely form… …and gently inserts a probe into her brain, letting a yellow light activate her locus coeruleus. Within moments, the princess awakes. Now THAT’S a kiss. I’ll admit, this post isn’t about sleeping beauty. Instead, it’s about sleep-wake transitions, and how they might work. And the answer involves an up and coming molecule, hypocretin (aka orexin), and an area of the brain called the locus coeruleus (LC). And it involves mice, who are little sleeping beauties in their own way. We’ll start with hypocretin (or orexin*). Hypocretin is a small peptide released from the hypothalamus of the brain. It’s a very recently discovered molecule (published in 1998), and has been enjoying a recent explosion in popularity, due to its interesting involvement in drug addiction and feeding behavior, and its very clear role in sleep. You see, hypocretin controls sleep/wake cycles by mediating what we call “arousal” (which is not that, though it’s that, too). Neurons that produce hypocretin are silent while you are asleep, but burst of firing and the release of hypocretin from these neurons comes immediately before wakefulness. And hypocretin is such a strong mediator of sleep/wake transitions that loss of hypocretin produces some very striking narcolepsy. © 2012 Scientific American

Keyword: Sleep
Link ID: 17411 - Posted: 10.23.2012