Chapter 10. Biological Rhythms and Sleep
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Helen Briggs Health editor, BBC News website Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's, research suggests. A study of older Canadian adults found that past benzodiazepine use for three months or more was linked to an increased risk (up to 51%) of dementia. NHS guidelines say the drugs should be used for eight to 12 weeks at most. The French-Canadian team says while the link is not definitive, it is another warning that treatments should not exceed three months. "Benzodiazepine use is associated with an increased risk of Alzheimer's disease," lead researcher, Sophie Billioti de Gage of the University of Bordeaux, France, and colleagues wrote in the BMJ. "Unwarranted long-term use of these drugs should be considered as a public health concern." The study involved about 2,000 cases of Alzheimer's disease in adults aged over 66 living in Quebec. All had been prescribed benzodiazepines. They were compared with about 7,000 healthy people of the same age living in the same community. While an increased risk was found in those on benzodiazepines, the nature of the link was unclear. Dr Eric Karran, director of research at Alzheimer's Research UK, said: "This study shows an apparent link between the use of benzodiazepines and Alzheimer's disease although it's hard to know the underlying reason behind the link. BBC © 2014
By Smitha Mundasad Health reporter, BBC News More than 300 people a year in the UK and Ireland report they have been conscious during surgery - despite being given general anaesthesia. In the largest study of its kind, scientists suggests this happens in one in every 19,000 operations. They found episodes were more likely when women were given general anaesthesia for Caesarean sections or patients were given certain drugs. Experts say though rare, much more needs to be done to prevent such cases. Led by the Royal College of Anaesthetists and Association of Anaesthetists of Great Britain and Ireland, researchers studied three million operations over a period of one year. More than 300 people reported they had experienced some level of awareness during surgery. Most episodes were short-lived and occurred before surgery started or after operations were completed. But some 41% of cases resulted in long-term psychological harm. Patients described a variety of experiences - from panic and pain to choking - though not all episodes caused concern. The most alarming were feelings of paralysis and being unable to communicate, the researchers say. One patient, who wishes to remain anonymous, described her experiences of routine orthodontic surgery at the age of 12. She said: "I could hear voices around me and I realised with horror that I had woken up in the middle of the operation but couldn't move a muscle. BBC © 2014
Greta Kaul, Stanford researchers say poor sleep may be an independent risk factor for suicide in adults over 65. Researchers used data from a previous epidemiological study to compare the sleep quality of 20 older adults who committed suicide and 400 who didn't, over 10 years. Researchers found that those who didn't sleep well were 1.4 times more likely to commit suicide within a decade. Older adults have disproportionately high suicide rates in the first place, especially older men. The Stanford researchers believe that on its own, sleeping poorly could be a risk factor for suicide later in life. It may even be a more powerful predictor of suicide risk than symptoms of depression. They found that the strongest predictor of suicide was the combination of bad sleep and depression. Unlike many biological, psychological and social risk factors for suicide, sleep disorders tend to be treatable, said Rebecca Bernert, the lead author of the study. Sleep disorders are also less stigmatized than other suicide risk factors. Bernert is now studying whether treating insomnia is effective in preventing depression and suicide. The study was published in JAMA Psychiatry in August. © 2014 Hearst Communications, Inc.
By Meeri Kim The pervasive glow of electronic devices may be an impediment to a good night’s sleep. That’s particularly noticeable now, when families are adjusting to early wake-up times for school. Teenagers can find it especially hard to get started in the morning. For nocturnal animals, it spurs activity. For daytime species such as humans, melatonin signals that it’s time to sleep. As lamps switch off in teens’ bedrooms across America, the lights from their computer screens, smartphones and tablets often stay on throughout the night. These devices emit light of all colors, but it’s the blues in particular that pose a danger to sleep. Blue light is especially good at preventing the release of melatonin, a hormone associated with nighttime. Ordinarily, the pineal gland, a pea-size organ in the brain, begins to release melatonin a couple of hours before your regular bedtime. The hormone is no sleeping pill, but it does reduce alertness and make sleep more inviting. However, light — particularly of the blue variety — can keep the pineal gland from releasing melatonin, thus warding off sleepiness. You don’t have to be staring directly at a television or computer screen: If enough blue light hits the eye, the gland can stop releasing melatonin. So easing into bed with a tablet or a laptop makes it harder to take a long snooze, especially for sleep-deprived teenagers who are more vulnerable to the effects of light than adults. During adolescence, the circadian rhythm shifts, and teens feel more awake later at night. Switching on a TV show or video game just before bedtime will push off sleepiness even later even if they have to be up by 6 a.m. to get to school on time.
|By Mark Fischetti Parents, students and teachers often argue, with little evidence, about whether U.S. high schools begin too early in the morning. In the past three years, however, scientific studies have piled up, and they all lead to the same conclusion: a later start time improves learning. And the later the start, the better. Biological research shows that circadian rhythms shift during the teen years, pushing boys and girls to stay up later at night and sleep later into the morning. The phase shift, driven by a change in melatonin in the brain, begins around age 13, gets stronger by ages 15 and 16, and peaks at ages 17, 18 or 19. Does that affect learning? It does, according to Kyla Wahlstrom, director of the Center for Applied Research and Educational Improvement at the University of Minnesota. She published a large study in February that tracked more than 9,000 students in eight public high schools in Minnesota, Colorado and Wyoming. After one semester, when school began at 8:35 a.m. or later, grades earned in math, English, science and social studies typically rose a quarter step—for example, up halfway from B to B+. Two journal articles that Wahlstrom has reviewed but have not yet been published reach similar conclusions. So did a controlled experiment completed by the U.S. Air Force Academy, which required different sets of cadets to begin at different times during their freshman year. A 2012 study of North Carolina school districts that varied school times because of transportation problems showed that later start times correlated with higher scores in math and reading. Still other studies indicate that delaying start times raises attendance, lowers depression rates and reduces car crashes among teens, all because they are getting more of the extra sleep they need. © 2014 Scientific American
Ever wonder why it’s hard to focus after a bad night’s sleep? Using mice and flashes of light, scientists show that just a few nerve cells in the brain may control the switch between internal thoughts and external distractions. The study, partly funded by the National Institutes of Health, may be a breakthrough in understanding how a critical part of the brain, called the thalamic reticular nucleus (TRN), influences consciousness. “Now we may have a handle on how this tiny part of the brain exerts tremendous control over our thoughts and perceptions,” said Michael Halassa, M.D., Ph.D., assistant professor at New York University’s Langone Medical Center and a lead investigator of the study. “These results may be a gateway into understanding the circuitry that underlies neuropsychiatric disorders.” The TRN is a thin layer of nerve cells on the surface of the thalamus, a center located deep inside the brain that relays information from the body to the cerebral cortex. The cortex is the outer, multi-folded layer of the brain that controls numerous functions, including one’s thoughts, movements, language, emotions, memories, and visual perceptions. TRN cells are thought to act as switchboard operators that control the flow of information relayed from the thalamus to the cortex. To understand how the switches may work, Dr. Halassa and his colleagues studied the firing patterns of TRN cells in mice during sleep and arousal, two states with very different information processing needs. The results published in Cell, suggest that the TRN has many switchboard operators, each dedicated to controlling specific lines of communication. Using this information, the researchers could alter the attention span of mice.
By Rachel Feltman At every waking moment, your brain is juggling two very different sets of information. Input from the world around you, like sights and smells, has to be processed. But so does internal information — your memories and thoughts. Right now, for example, I’m looking at a peach: It’s yellow and pink, and has a lot of fuzz. But I also know that it smells nice (a personal assessment) and I’m imagining how good it will taste, based on my previous experience with fragrant pink fruits. The brain’s ability to handle these different signals is key to cognitive function. In some disorders, particularly autism and schizophrenia, this ability is disrupted. The brain has difficulty keeping internal and external input straight. In a new study published Thursday in Cell, researchers observe the switching method in action for the first time. While the research used mice, not humans, principal investigator and NYU Langone Medical Center assistant professor Michael Halassa sees this as a huge step toward understanding and manipulating the same functions in humans. “This is one of the few moments in my life where I’d actually say yes, absolutely this is going to translate to humans,” Halassa said. “This isn’t something based on genes or molecules that are specific to one organism. The underlying principles of how the brain circuitry works are likely to be very similar in humans and mice.” That circuitry has been hypothesized for decades. Neurologists know that the cortex of the brain is responsible for higher cognitive functions, like music and language. And the thalamus, which is an egg-like structure in the center of the brain, works to direct the flow of internal and external information before it gets to the cortex.
The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.
|By Piercarlo Valdesolo In the summer of 2009 I tried to cure homemade sausages in my kitchen. One of the hazards of such a practice is preventing the growth of undesirable molds and diseases such as botulism. My wife was not on board with this plan, skeptical of my ability to safely execute the procedure. And so began many weeks of being peppered with warnings, relevant articles and concerned looks. When the time came for my first bite, nerves were high. My throat itched. My heart raced. My vision blurred. I had been botulized! Halfway through our walk to the hospital I regained my composure. Of course I had not been instantaneously struck by an incredibly rare disease that, by the way, takes at least 12 hours after consumption to manifest and does not share many symptoms with your garden variety anxiety attack. My experience had been shaped by my mindset. A decade of learning about the psychological power of expectations could not inoculate me from its effect. Psychologists know that beliefs about how experiences should affect us can bring about the expected outcomes. Though these “placebo effects” have primarily been studied in the context of pharmaceutical interventions (e.g. patients reporting pain relief after receiving saline they believed to be an analgesic), recent research has shown their strength in a variety of domains. Tell people that their job has exercise benefits and they will lose more weight than their coworkers who had no such belief. Convince people of a correlation between athleticism and visual acuity and they will show better vision after working out . Trick people into believing they are consuming caffeine and their vigilance and cognitive functioning increases. Some evidence shows that such interventions can even mitigate the negative effects of other experiences. For example, consuming placebo caffeine alleviates the cognitive consequences of sleep deprivation. © 2014 Scientific American
Emily Underwood Since swine flu swept the globe in 2009, scientists have scrambled to determine why a small percentage of children in Europe who received the flu vaccine Pandemrix developed narcolepsy, an incurable brain disorder that causes irresistible sleepiness. This week, a promising explanation was dealt a setback when prominent sleep scientist Emmanuel Mignot of Stanford University in Palo Alto, California, and colleagues retracted their influential study reporting a potential link between the H1N1 virus used to make the vaccine and narcolepsy. Some researchers were taken aback. “This was one of the most important pieces of work on narcolepsy that has come out,” says neuroimmunologist Lawrence Steinman, a close friend and colleague of Mignot’s, who is also at Stanford. The retraction, announced in Science Translational Medicine (STM), “really caught me by surprise,” he says. Others say that journal editors should have detected problems with the study’s methodology. The work provided the first substantiation of an autoimmune mechanism for narcolepsy, which could explain the Pandemrix side effect, researchers say. The vaccine, used only in Europe, seems to have triggered the disease in roughly one out of 15,000 children who received it. The affected children carried a gene variant for a particular human leukocyte antigen (HLA) type—a molecule that presents foreign proteins to immune cells—considered necessary for developing narcolepsy. In the 18 December 2013 issue of STM, Mignot and colleagues reported that T cells from people with narcolepsy, but not from healthy controls, are primed to attack by hypocretin, a hormone that regulates wakefulness. They also showed molecular similarities between fragments of the H1N1 virus and the hypocretin molecule and suggested that these fragments might fool the immune system into attacking hypocretin-producing cells. © 2014 American Association for the Advancement of Science
By PAULA SPAN Call me nuts, but I want to talk more about sleeping pill use. Hold your fire for a few paragraphs, please. Just a week after I posted here about medical efforts to help wean older patients off sleeping pills — causing a flurry of comments, many taking exception to the whole idea as condescending or dismissive of the miseries of insomnia — researchers at the Centers for Disease Control and Prevention and Johns Hopkins published findings that reinforce concerns about these drugs. I say “reinforce” because geriatricians and other physicians have fretted for years about the use of sedative-hypnotic medications, including benzodiazepines (like Ativan, Klonopin, Xanax and Valium) and the related “Z-drugs” (like Ambien) for treating insomnia. “I’m not comfortable writing a prescription for these medications,” said Dr. Cara Tannenbaum, the geriatrician at the University of Montreal who led the weaning study. “I haven’t prescribed a sedative-hypnotic in 15 years.” In 2013, the American Geriatrics Society put sedative-hypnotics on its first Choosing Wisely campaign list of “Five Things Physicians and Patients Should Question,” citing heightened fall and fracture risks and automobile accidents in older patients who took them. Now the C.D.C. has reported that a high number of emergency room visits are associated with psychiatric medications in general, and zolpidem — Ambien — in particular. They’re implicated in 90,000 adult E.R. visits annually because of adverse reactions, the study found; more than 19 percent of those visits result in hospital admissions. Among those taking sedatives and anxiety-reducing drugs, “a lot of visits were because people were too sleepy or hard to arouse, or confused,” said the lead author, Dr. Lee Hampton, a medical officer at the C.D.C. “And there were also a lot of falls.” © 2014 The New York Times Company
|By Jillian Rose Lim and LiveScience People who don't get enough sleep could be increasing their risk of developing false memories, a new study finds. In the study, when researchers compared the memory of people who'd had a good night's sleep with the memory of those who hadn't slept at all, they found that, under certain conditions, sleep-deprived individuals mix fact with imagination, embellish events and even "remember" things that never actually happened. False memories occur when people's brains distort how they remember a past event — whether it's what they did after work, how a painful relationship ended or what they witnessed at a crime scene. Memory is not an exact recording of past events, said Steven Frenda, a psychology Ph.D. student at the University of California, Irvine, who was involved in the study. Rather, fresh memories are constructed each time people mentally revisit a past event. During this process, people draw from multiple sources — like what they've been told by others, what they've seen in photographs or what they know as stereotypes or expectations, Frenda said. The new findings "have implications for people's everyday lives —recalling information for an exam, or in work contexts, but also for the reliability of eyewitnesses who may have experienced periods of restricted or deprived sleep," said Frenda, who noted that chronic sleep deprivation is on the rise. In a previous study, Frenda and his colleagues observed that people with restricted sleep (less than 5 hours a night) were more likely to incorporate misinformation into their memories of certain photos, and report they had seen video footage of a news event that didn't happen. In the current study, they wanted to see how a complete lack of sleep for 24 hours could influence a person's memory. © 2014 Scientific American
By James Gallagher Health editor, BBC News website Even low levels of light in bedrooms may stop breast cancer drugs from working, US researchers have warned. Animal tests showed light, equivalent to that from street lamps, could lead to tumours becoming resistant to the widely used drug Tamoxifen. The study, published in the journal Cancer Research, showed the light affected sleep hormones, which in turn altered cancer cell function. UK experts said it was an intriguing finding, but not proven in people. Tamoxifen has transformed the treatment of breast cancer by extending lives and increasing survival times. It stops the female hormone oestrogen fuelling the growth of tumours although the cancerous cells may eventually become resistant to the drug. Light Researchers at the Tulane University School of Medicine investigated the role of the body clock in Tamoxifen resistance. They focused their research on the sleep-promoting hormone melatonin, which normally begins to rise in the evening and continues through the night, before falling away as dawn approaches. However, light in the evening - such as from a smartphone, tablet or artificial lights - can lower melatonin levels. Rats, with human breast cancer and treated with Tamoxifen, were left to sleep in a completely dark cage or one that had dim light. The scientists showed that in dim light, melatonin levels were lower, the tumours were bigger and were resistant to Tamoxifen. A second set of tests showed that giving those mice melatonin supplements kept Tamoxifen working and resulted in smaller tumours. BBC © 2014
Keyword: Biological Rhythms
Link ID: 19881 - Posted: 07.26.2014
By DONALD G. MCNEIL Where was I? Sorry — must have nodded off for a decade. Ten years ago, I spent two nights in a sleep lab at SUNY Downstate Medical Center, taking the test for sleep apnea, and wrote about it for Science Times. Back then, “sleep technicians” wired me up like the Bride of Frankenstein: 15 sensors glued or clamped to my scalp, lip, eye sockets, jaw, index finger, chest and legs, two belts around my torso, and a “snore mike” on my neck. As I slept, an infrared camera watched over me. And I ended up spending 23 hours in that hospital bed because the test wasn’t over until you could lie in a dark room for 20 minutes without dozing off. I had such a sleep deficit that I kept conking out, not just all night, but all the next day. So this year, when a company called NovaSom offered to let me try out a new home sleep-test kit that promises to streamline the process, I said yes. In the decade since my ordeal, the pendulum has swung sharply in the direction of the home test, said Dr. M. Safwan Badr, past president of the American Academy of Sleep Medicine, which first recognized home testing for apnea in 2007. Insurers prefer it because it costs only about $300, about one-tenth that of a hospital test, and many patients like it, too. “Lots of people are reluctant to let a stranger watch them sleep,” said Dr. Michael Coppola, a former president of the American Sleep Apnea Association who is now the chief medical officer at NovaSom. Doctors estimate that 18 million Americans have moderate to severe apnea and 75 percent of them do not know it. Home testing is not recommended for those with heart failure, emphysema, seizures and a few other conditions. And because it does not record brain waves as a hospital lab does, a home test can be fooled by someone who just lies awake all night staring at the ceiling. But it’s useful for many people who exhibit the warning signs of apnea, such as waking up exhausted after a full night’s sleep or dozing off at the wheel in bright daylight. And severe apnea can be lethal: starving the brain of oxygen all night quadruples the risk of stroke. © 2014 The New York Times Company
Link ID: 19865 - Posted: 07.22.2014
By Kelly Clancy In one important way, the recipient of a heart transplant ignores its new organ: Its nervous system usually doesn’t rewire to communicate with it. The 40,000 neurons controlling a heart operate so perfectly, and are so self-contained, that a heart can be cut out of one body, placed into another, and continue to function perfectly, even in the absence of external control, for a decade or more. This seems necessary: The parts of our nervous system managing our most essential functions behave like a Swiss watch, precisely timed and impervious to perturbations. Chaotic behavior has been throttled out. Or has it? Two simple pendulums that swing with perfect regularity can, when yoked together, move in a chaotic trajectory. Given that the billions of neurons in our brain are each like a pendulum, oscillating back and forth between resting and firing, and connected to 10,000 other neurons, isn’t chaos in our nervous system unavoidable? The prospect is terrifying to imagine. Chaos is extremely sensitive to initial conditions—just think of the butterfly effect. What if the wrong perturbation plunged us into irrevocable madness? Among many scientists, too, there is a great deal of resistance to the idea that chaos is at work in biological systems. Many intentionally preclude it from their models. It subverts computationalism, which is the idea that the brain is nothing more than a complicated, but fundamentally rule-based, computer. Chaos seems unqualified as a mechanism of biological information processing, as it allows noise to propagate without bounds, corrupting information transmission and storage. © 2014 Nautilus,
Keyword: Biological Rhythms
Link ID: 19859 - Posted: 07.21.2014
by Azeen Ghorayshi Food could be a new weapon in shaking off the effects of jet lag after research in mice showed that the insulin released as a result of eating can be a key factor in restoring a disrupted body clock. Miho Sato and her colleagues at The Research Institute for Time Studies at Yamaguchi University in Japan did experiments in mice and tissue cultures to show, for the first time, that increases in insulin affect circadian rhythms. These daily rhythms affect alertness, sleep patterns, and mediate many other physiological processes. Your biological clock is regulated by two broad factors: first, the central rhythm is reset daily by light, as sensory input from the eyes is processed by a small part of the brain called the suprachiasmatic nucleus. The rise and fall of hormones linked to sleep, for example, match this rhythm. But circadian rhythms are also present in peripheral "clocks" in a wide range of cell types in the body. Some of these can be influenced by food. Sato demonstrated the role of insulin by shifting the peripheral body clock in the livers of mice by feeding them only at night. They then split the mice into two groups, supressed insulin levels in one group, and returned all the mice to daytime feeding. Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver-gene expression. The livers of the insulin-suppressed mice had still not returned to normal. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 19830 - Posted: 07.15.2014
|By William Skaggs Jet lag is a pain. Besides the inconvenience and frustration of traveling more than a few time zones, jet lag likely causes billions of dollars in economic losses. The most effective treatment, according to much research, is structured exposure to light, although the drug melatonin may also sometimes be helpful at bedtime. Both approaches have been used for more than 20 years, and during that time no viable new interventions have appeared. Recently, however, research into the molecular biology of circadian rhythms has raised the prospect of developing new drugs that might produce better results. Jet lag occurs when the “biological clock” in the brain becomes misaligned with the local rhythm of daily activity. The ultimate goal of circadian medicine is a treatment that instantly resets the brain's clock. Failing that, it would be helpful to have treatments that speed the rate of adjustment. Four recent discoveries suggest new possibilities. The first involves vasopressin, which is the main chemical signal used to synchronize cellular rhythms of activity in the brain area that is responsible for our biological clock. Blocking vasopressin makes it much easier to reset this clock. Potentially, a drug that interferes with vasopressin could work as a fast-acting treatment for jet lag. The second and third possibilities involve a pair of brain chemicals called salt-inducible kinase 1 (SIK1) and casein kinase 1ε (CK1ε), both of which limit the ability of light to reset the brain's clock. Drugs already exist that interfere with their action and greatly increase the effectiveness of light exposure. The existing drugs are not viable jet-lag treatments, because they are hard to administer and have unpleasant side effects, but researchers hope better drugs can be developed that work in a similar way. © 2014 Scientific American,
By Fredrick Kunkle Sleep disturbances such as apnea may increase the risk of Alzheimer’s disease, while moderate exercise in middle age and mentally stimulating games, such as crossword puzzles, may prevent the onset of the dementia-causing disease, according to new research to be presented Monday. The findings — which are to be introduced during the six-day Alzheimer’s Association International Conference in Copenhagen — bolster previous studies that suggest sleep plays a critical role in the aging brain’s health, perhaps by allowing the body to cleanse itself of Alzheimer's-related compounds during down time. The studies also add to a growing body of literature that suggests keeping the brain busy keeps it healthy. The battle against Alzheimer’s disease has become more urgent for the United States and other developing nations as their populations turn increasingly gray. The disease is the leading cause of dementia in older people and afflicts more than 5 million Americans. At its current pace, the number is expected to soar to 16 million people by 2050. In 2012, the United States adopted a national plan to combat the disease and the G-8 nations last year adopted a goal of providing better treatment and prevention by 2025. Erin Heintz, a spokeswoman for the Alzheimer’s Association, said U.S. government funding to combat the disease now stands at about $500 million a year. To reach its 2025 goal, the United States should be spending $2 billion a year, she said.
Carmen Fishwick Do you have difficulty getting enough sleep? Sleep problems affect one in three of us at any one time, and about 10% of the population on a chronic basis. Of Guardian readers who responded to a recent poll, 23% reported that they sleep between four and six hours a night. With continued lack of sufficient sleep, the part of the brain that controls language and memory is severely impaired, and 17 hours of sustained wakefulness is equivalent to performing on a blood alcohol level of 0.05% – the UK's legal drink driving limit. In 2002, American researchers analysed data from more than one million people, and found that getting less than six hours' sleep a night was associated with an early demise – as was getting over eight hours. Studies have found that blood pressure is more than three times greater among those who sleep for less than six hours a night, and women who have less than four hours of sleep are twice as likely to die from heart disease. Other research suggests that a lack of sleep is also related to the onset of diabetes, obesity, and cancer. Are you worried about how much sleep you get? Professor Russell Foster, chair of circadian neuroscience and head of the Sleep and Circadian Neuroscience Institute at the University of Oxford, and professor Colin Espie, professor of sleep medicine at the University of Oxford and lead researcher on the Great British Sleep Survey, answered reader questions. © 2014 Guardian News and Media Limited
Link ID: 19724 - Posted: 06.14.2014
by Moheb Costandi Rest easy after learning a new skill. Experiments in mice suggest that a good night's sleep helps us lay down memories by promoting the growth of new connections between brain cells. Neuroscientists believe that memory involves the modification of synapses, which connect brain cells, and numerous studies published over the past decade have shown that sleep enhances the consolidation of newly formed memories in people. But exactly how these observations were related was unclear. To find out, Wenbiao Gan of the Skirball Institute of Biomolecular Medicine at New York University Medical School and his colleagues trained 15 mice to run backwards or forwards on a rotating rod. They allowed some of them to fall asleep afterwards for 7 hours, while the rest were kept awake. The team monitored the activity and microscopic structure of the mice's motor cortex, the part of the brain that controls movement, through a small transparent "window" in their skulls. This allowed them to watch in real time how the brain responded to learning the different tasks. Sprouting spines They found that learning a new task led to the formation of new dendritic spines – tiny structures that project from the end of nerve cells and help pass electric signals from one neuron to another – but only in the mice left to sleep. This happened during the non-rapid eye movement stage of sleep. Each task caused a different pattern of spines to sprout along the branches of the same motor cortex neurons. © Copyright Reed Business Information Ltd.