Posts tagged sleep
Articles and news from the latest research reports.
Quality of waking hours determines ease of falling asleep
The quality of wakefulness affects how quickly a mammal falls asleep, UT Southwestern Medical Center researchers report in a study that identifies two proteins never before linked to alertness and sleep-wake balance.
“This study supports the idea that subjective sleepiness is influenced by the quality of experiences right before bedtime. Are you reluctantly awake or excited to be awake?” said Dr. Masashi Yanagisawa, professor of molecular genetics and a Howard Hughes Medical Institute investigator at UT Southwestern. He is principal author of the study published online in May in the Proceedings of the National Academy of Sciences.
Co-author Dr. Robert Greene, UT Southwestern professor of psychiatry and a physician at the Dallas VA Medical Center, said the study is unique in showing that the need for sleep (called sleep homeostasis) can be separated from wakefulness both behaviorally and biochemically, meaning the two processes can now be studied individually.
“Two of the great mysteries in neuroscience are why do we sleep and what is sleep’s function? Separating sleep need from wakefulness and identifying two different proteins involved in these steps represents a fundamental advance,” he said.
If borne out by further research, this study could lead to new ways of assessing and possibly treating sleep disorders, perhaps by focusing more attention on the hours before bedtime because the quality of wakefulness has a profound effect on sleep, Dr. Yanagisawa said.
The experiment featured three groups of mice with virtually identical genes. The control group slept and woke at will and followed the usual mouse pattern of sleeping during the day and being awake at night. The two test groups were treated the same and had the same amount of sleep delay – six hours – but they were kept awake in different ways, said lead author Dr. Ayako Suzuki, a postdoctoral researcher who works in the laboratories of both Dr. Yanagisawa and Dr. Greene.
The first test group’s sleep was delayed by a series of cage changes. Mice are intensely curious, so each cage change was followed by an hour spent vigorously exploring the new surroundings. This behavior would roughly correspond to teenagers voluntarily delaying bedtime with a new and stimulating event like a rock concert or video game.
Researchers kept the second group awake as gently as possible, usually by waving a hand in front of the cage or tapping it lightly whenever the mice appeared to be settling down to sleep. That test group would more resemble parents reluctantly staying awake awaiting a child’s return from a concert.
Both test groups experienced the same amount of sleep deprivation, but their reactions to the different forms of alertness were striking, Dr. Yanagisawa said. In one test, the cage-changing group took longer to fall asleep than the gentle-handling group even though an analysis of their brain waves indicated equal amounts of sleep need in both test groups.
“The need to sleep is as high in the cage-changing group as in the gentle-handling group, but the cage-changers didn’t feel sleepy at all. Their time to fall asleep was nearly the same as the free-sleeping, well-rested control group,” he said.
The researchers identified two proteins that affected these responses, each linked to different aspects of sleep: phosphorylated dynamin 1 levels were linked to how long it took to fall asleep, while phosphorylated N-myc downstream regulated gene 2 protein levels tracked the amount of sleep deprivation and corresponded to the well-known brain-wave measure of sleep need, they report.
“The two situations are different biochemically, which is a novel finding,” Dr. Yanagisawa said, adding, “These proteins are completely new to sleep research and have never before been linked to sleep need and wakefulness.”
From an evolutionary perspective, an arousal mechanism that adapts to environmental stimuli is crucial because sleeping on a rigid schedule could be dangerous. “Animals, including humans, must be able to keep themselves at least temporarily alert, say during a natural disaster,” he said.
(Image: Robert Manella / Getty Images)
Sleep Mechanism Identified That Plays Role in Emotional Memory
Sleep researchers from University of California campuses in Riverside and San Diego have identified the sleep mechanism that enables the brain to consolidate emotional memory and found that a popular prescription sleep aid heightens the recollection of and response to negative memories.
Their findings have implications for individuals suffering from insomnia related to posttraumatic stress disorder (PTSD) and other anxiety disorders who are prescribed zolpidem (Ambien) to help them sleep.
The study — “Pharmacologically Increasing Sleep Spindles Enhances Recognition for Negative and High-arousal Memories” — appears in the Journal of Cognitive Neuroscience. It was funded by a National Institutes of Health career award to Sara C. Mednick, assistant professor of psychology at UC Riverside, of $651,999 over five years.
Mednick and UC San Diego psychologists Erik J. Kaestner and John T. Wixted determined that a sleep feature known as sleep spindles — bursts of brain activity that last for a second or less during a specific stage of sleep — are important for emotional memory.
Research Mednick published earlier this year demonstrated the critical role that sleep spindles play in consolidating information from short-term to long-term memory in the hippocampus, located in the cerebral cortex of the brain. Zolpidem enhanced the process, a discovery that could lead to new sleep therapies to improve memory for aging adults and those with dementia, Alzheimer’s and schizophrenia. It was the first study to show that sleep can be manipulated with pharmacology to improve memory.
“We know that sleep spindles are involved in declarative memory — explicit information we recall about the world, such as places, people and events, ” she explained.
But until now, researchers had not considered sleep spindles as playing a role in emotional memory , focusing instead on rapid eye movement (REM) sleep.
Using two commonly prescribed sleep aids — zolpidem and sodium oxybate (Xyrem) — Mednick, Kaestner and Wixted were able to tease apart the effects of sleep spindles and rapid eye movement (REM) sleep on the recall of emotional memories. They determined that sleep spindles, not REM, affect emotional memory.
The researchers gave zolpidem, sodium oxybate (Xyrem) and a placebo to 28 men and women between the ages of 18 and 39 who were normal sleepers, allowing several days between doses to allow the pharmaceuticals to leave their bodies. The participants viewed standardized images known to elicit positive and negative responses for one second before and after taking supervised naps. They recalled more images that had negative or highly arousing content after taking zolpidem, a finding that also suggests that the brain may favor consolidation of negative memories, she said.
“I was surprised by the specificity of the results, that the emotional memory improvement was specifically for the negative and high-arousal memories, and the ramifications of these results for people with anxiety disorders and PTSD,” Mednick said. “These are people who already have heightened memory for negative and high-arousal memories. Sleep drugs might be improving their memories for things they don’t want to remember.”
The study may have even broader implications, the researchers said. Clinical guidelines of the U.S. Department of Veterans Affairs and Department of Defense recommend against the routine use of benzodiazepines to treat PTSD, although their use increased among men and women with PTSD between 2003 and 2010. The effects of benzodiazepines on sleep are similar to those of zolpidem.
The U.S. Air Force uses zolpidem as one of the prescribed “no-go pills” to help flight crews calm down after taking stimulants to stay awake during long missions, the researchers noted in the study.
“In light of the present results, it would be worthwhile to investigate whether the administration of benzodiazepine-like drugs may be increasing the retention of highly arousing and negative memories, which would have a countertherapeutic effect,” they wrote. “Further research on the relationship between hypnotics and emotional mood disorders would seem to be in order.”
(Source: ucrtoday.ucr.edu)
PD-Like Sleep and Motor Problems Observed in α-Synuclein Mutant Mice
The presence of Lewy bodies in nerve cells, formed by intracellular deposits of the protein α-synuclein, is a characteristic pathologic feature of Parkinson’s Disease (PD). In the quest for an animal model of PD that mimics motor and non-motor symptoms of human PD, scientists have developed strains of mice that overexpress α-synuclein. By studying a strain of mice bred to overexpress α-synuclein via the Thy-1 promoter, scientists have found these mice develop many of the age-related progressive motor symptoms of PD and demonstrate changes in sleep and anxiety. Their results are published in the latest issue of Journal of Parkinson’s Disease.
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most obvious symptoms are movement-related, such as involuntary shaking and muscle stiffness; non-motor symptoms, such as increases in anxiety and sleep disturbances, can appear prior to the onset of motor symptoms. Although the drug levodopa can relieve some symptoms, there is no cure – intensifying the pressure to find an animal model that can help clarify the pathological processes underlying human PD and find new medications to treat the pathology and/or relieve symptoms.
Investigators at the National Institute on Aging compared wild type mice with specially bred mice that were transgenic for the A53T mutation of the human α-synuclein (SNCA) gene under the control of a human thymus cell antigen 1, theta (THY-1) promoter. As the mice aged, their motor performance on a rotarod test (which measures how long the mouse can remain on a rotating rod) became impaired and the length of their strides were significantly shorter than the wild type control mice.
The study also found that SNCA mice displayed fragmented nighttime activity patterns compared to wild type controls and appeared to have a reduced overall sleep time. “Despite the prevalence of abnormal sleep patterns in PD, very few studies to date have outlined sleep disturbances in animal models of PD,” says Sarah M. Rothman, PhD, a researcher with the National Institute on Aging, in Baltimore, MD.
Many PD patients typically show an increase in anxiety and depression, and in this respect the SNCA mouse model did not replicate the human condition. SNCA mice displayed an early and significant decrease in anxiety-like behavior that persisted throughout their lifespan, as shown by both open field and elevated plus maze tests (in which mice have the choice of spending time in open or closed arms of a maze). Other rodent models that utilize changes in expression of α-synuclein have also reported lower anxiety levels. The authors suggest that higher levels of serotonin found in the hypothalamus of the SNCA mice may be associated with the reduced anxiety observed.
The authors say it is important to remember that the SNCA “model utilizes the presence of a mutation that only occurs very rarely in PD. While all PD patients display α-synuclein pathology, they do not all express the mutated form of the protein,” says Dr. Rothman.
(Source: alphagalileo.org)
All mammals sleep, as do birds and some insects. However, how this basic function is regulated by the brain remains unclear. According to a new study by researchers from the RIKEN Brain Science Institute, a brain region called the lateral habenula plays a central role in the regulation of REM sleep. In an article published today in the Journal of Neuroscience, the team shows that the lateral habenula maintains and regulates REM sleep in rats through regulation of the serotonin system. This study is the first to show a role of the lateral habenula in linking serotonin metabolism and sleep.
The lateral habenula is a region of the brain known to regulate the metabolism of the neurotransmitter serotonin in the brain and to play a key role in cognitive functions.
“Serotonin plays a central role in the pathophysiology of depression, however, it is not clear how abnormalities in regulation of serotonin metabolism in the brain lead to symptoms such as insomnia in depression,” explain Dr. Hidenori Aizawa and Dr. Hitoshi Okamoto who led the study.
Since animals with increased serotonergic activity at the synapse experienced less REM sleep, the researchers hypothesized that the lateral habenula, which regulates serotonergic activity in the brain, must modulate the duration of REM sleep.
They show that removing the lateral habenula in rats results in a reduction of theta rhythm, an oscillatory activity that appears during REM sleep, in the hippocampus, and shortens the rats’ REM sleep periods. However, this inhibitory effect of the lateral habenular lesion on REM sleep disappears when the serotonergic neurons in the midbrain are lesioned.
The team recorded neural activity simultaneously in the lateral habenula and hippocampus in a sleeping rat. They find that the lateral habenular neurons, which fire persistently during non-REM sleep, begin to fire rhythmically in accordance with the theta rhythm in the hippocampus when the animal is in REM sleep.
“Our results indicate that the lateral habenula is essential for maintaining theta rhythms in the hippocampus, which characterize REM sleep in the rat, and that this is done via serotonergic modulation,” concludes Dr Aizawa.
“This study reveals a novel role of the lateral habenula, linking serotonin and REM sleep, which suggests that an hyperactive habenula in patients with depression may cause altered REM sleep,” add the authors.
Restless Legs Syndrome, Insomnia And Brain Chemistry: A Tangled Mystery Solved?
Johns Hopkins researchers believe they may have discovered an explanation for the sleepless nights associated with restless legs syndrome (RLS), a symptom that persists even when the disruptive, overwhelming nocturnal urge to move the legs is treated successfully with medication.
Neurologists have long believed RLS is related to a dysfunction in the way the brain uses the neurotransmitter dopamine, a chemical used by brain cells to communicate and produce smooth, purposeful muscle activity and movement. Disruption of these neurochemical signals, characteristic of Parkinson’s disease, frequently results in involuntary movements. Drugs that increase dopamine levels are mainstay treatments for RLS, but studies have shown they don’t significantly improve sleep. An estimated 5 percent of the U.S. population has RLS.
The small new study, headed by Richard P. Allen, Ph.D., an associate professor of neurology at the Johns Hopkins University School of Medicine, used MRI to image the brain and found glutamate — a neurotransmitter involved in arousal — in abnormally high levels in people with RLS. The more glutamate the researchers found in the brains of those with RLS, the worse their sleep.
The findings are published in the May issue of the journal Neurology.
“We may have solved the mystery of why getting rid of patients’ urge to move their legs doesn’t improve their sleep,” Allen says. “We may have been looking at the wrong thing all along, or we may find that both dopamine and glutamate pathways play a role in RLS.”
For the study, Allen and his colleagues examined MRI images and recorded glutamate activity in the thalamus, the part of the brain involved with the regulation of consciousness, sleep and alertness. They looked at images of 28 people with RLS and 20 people without. The RLS patients included in the study had symptoms six to seven nights a week persisting for at least six months, with an average of 20 involuntary movements a night or more.
The researchers then conducted two-day sleep studies in the same individuals to measure how much rest each person was getting. In those with RLS, they found that the higher the glutamate level in the thalamus, the less sleep the subject got. They found no such association in the control group without RLS.
Previous studies have shown that even though RLS patients average less than 5.5 hours of sleep per night, they rarely report problems with excessive daytime sleepiness. Allen says the lack of daytime sleepiness is likely related to the role of glutamate, too much of which can put the brain in a state of hyperarousal — day or night.
If confirmed, the study’s results may change the way RLS is treated, Allen says, potentially erasing the sleepless nights that are the worst side effect of the condition. Dopamine-related drugs currently used in RLS do work, but many patients eventually lose the drug benefit and require ever higher doses. When the doses get too high, the medication actually can make the symptoms much worse than before treatment. Scientists don’t fully understand why drugs that increase the amount of dopamine in the brain would work to calm the uncontrollable leg movement of RLS.
Allen says there are already drugs on the market, such as the anticonvulsive gabapentin enacarbil, that can reduce glutamate levels in the brain, but they have not been given as a first-line treatment for RLS patients.
RLS wreaks havoc on sleep because lying down and trying to relax activates the symptoms. Most people with RLS have difficulty falling asleep and staying asleep. Only getting up and moving around typically relieves the discomfort. The sensations range in severity from uncomfortable to irritating to painful.
“It’s exciting to see something totally new in the field — something that really makes sense for the biology of arousal and sleep,” Allen says.
As more is understood about this neurobiology, the findings may not only apply to RLS, he says, but also to some forms of insomnia.
(Source: hopkinsmedicine.org)
Unusual comparison nets new sleep loss marker
For years, Paul Shaw, PhD, a researcher at Washington University School of Medicine in St. Louis, has used what he learns in fruit flies to look for markers of sleep loss in humans.
Shaw reverses the process in a new paper, taking what he finds in humans back to the flies and gaining new insight into humans as a result: identification of a human gene that is more active after sleep deprivation.
“I’m calling the approach cross-translational research,” says Shaw, associate professor of neurobiology. “Normally we go from model to human, but there’s no reason why we can’t take our studies from human to model and back again.”
Shaw and his colleagues plan to use the information they are gaining to create a panel of tests for sleep loss. The tests may one day help assess a person’s risk of falling asleep at the wheel of a car or in other dangerous contexts.
PLOS One published the results on April 24.
Scientists have known for years that sleep disorders and disruption raise blood serum levels of interleukin 6, an inflammatory immune compound. Shaw showed that this change is also detectable in saliva samples from sleep-deprived rats and humans.
Based on this link, Shaw tested the activity of other immune proteins in humans to see if any changed after sleep loss. The scientists took saliva samples from research participants after they had a normal night’s sleep and after they stayed awake for 30 hours. They found two immune genes whose activity levels rose during sleep deprivation.
“Normally we would do additional human experiments to verify these links,” Shaw says. “But those studies can be quite expensive, so we thought we’d test the connections in flies first.”
The researchers identified genes in the fruit fly that were equivalent to the human genes, but their activity didn’t increase when flies lost sleep. When they screened other, similar fruit fly genes, though, the scientists found one that did.
“We’ve seen this kind of switch happen before as we compared families of fly genes and families of human genes,” Shaw says. “Sometimes the gene performing a particular role will change, but the task will still be handled by a gene in the same family.”
When the scientists looked for the human version of the newly identified fly marker for sleep deprivation, they found ITGA5 and realized it hadn’t been among the human immune genes they screened at the start of the study. Testing ITGA5 activity in the saliva samples revealed that its activity levels increased during sleep deprivation.
“We will need more time to figure out how useful this particular marker will be for detecting sleep deprivation in humans,” Shaw says. “In the meantime, we’re going to continue jumping between our flies and humans to maximize our insights.”
Scientists probe the source of a pulsing signal in the sleeping brain
New findings clarify where and how the brain’s “slow waves” originate. These rhythmic signal pulses, which sweep through the brain during deep sleep at the rate of about one cycle per second, are assumed to play a role in processes such as consolidation of memory. For the first time, researchers have shown conclusively that slow waves start in the cerebral cortex, the part of the brain responsible for cognitive functions. They also found that such a wave can be set in motion by a tiny cluster of neurons.
"The brain is a rhythm machine, producing all kinds of rhythms all the time," says Prof. Arthur Konnerth of the Technische Universitaet Muenchen (TUM). "These are clocks that help to keep many parts of the brain on the same page." One such timekeeper produces the so-called slow waves of deep sleep, which are thought to be involved in transmuting fragments of a day’s experience and learning into lasting memory. They can be observed in very early stages of development, and they may be disrupted in diseases such as Alzheimer’s.
Previous studies, relying mainly on electrical measurements, have lacked the spatial resolution to map the initiation and propagation of slow waves precisely. But using light, Konnerth’s Munich-based team – in collaboration with researchers at Stanford and the University of Mainz – could both stimulate slow waves and observe them in unprecedented detail. One key result confirmed that the slow waves originate only in the cortex, ruling out other long-standing hypotheses. “The second major finding,” Konnerth says, “was that out of the billions of cells in the brain, it takes not more than a local cluster of fifty to one hundred neurons in a deep layer of the cortex, called layer 5, to make a wave that extends over the entire brain.”
New light on a fundamental neural mechanism
Despite considerable investigation of the brain’s slow waves, definitive answers about the underlying circuit mechanism have remained elusive. Where is the pacemaker for this rhythm? Where do the waves start, and where do they stop? This study – based on optical probing of intact brains of live mice under anesthesia – now provides the basis for a detailed, comprehensive view.
"We implemented an optogenetic approach combined with optical detection of neuronal activity to explore causal features of these slow oscillations, or Up-Down state transitions, that represent the dominating network rhythm in sleep," explains Prof. Albrecht Stroh of the Johannes Gutenberg University Mainz. Optogenetics is a novel technique that enabled the researchers to insert light-sensitive channels into specific kinds of neurons, to make them responsive to light stimulation. This allowed for selective and spatially defined stimulation of small numbers of cortical and thalamic neurons.
Access to the brain via optical fibers allowed for both microscopic recording and direct stimulation of neurons. Flashes of light near the mouse’s eyes were also used to stimulate neurons in the visual cortex. By recording the flux of calcium ions, a chemical signal that can serve as a more spatially precise readout of the electric activity, the researchers made the slow waves visible. They also correlated optical recordings with more conventional electrical measurements. As a result, it was possible to watch individual wave fronts spread – like ripples from a rock thrown into a quiet lake – first through the cortex and then through other brain structures.
A new picture begins to emerge: Not only is it possible for a tiny local cluster of neurons to initiate a slow wave that will spread far and wide, recruiting multiple regions of the brain into a single event – this appears to be typical. “In spontaneous conditions,” Konnerth says, “as it happens with you and me and everyone else every night in deep sleep, every part of the cortex can be an initiation site.” Furthermore, a surprisingly simple communication protocol can be seen in the slow wave rhythm. During each one-second cycle a single neuron cluster sends its signal and all others are silenced, as if they are taking turns bathing the brain in fragments of experience or learning, building blocks of memory. The researchers view these findings as a step toward a better understanding of learning and memory formation, a topic Konnerth’s group is investigating with funding from the European Research Council. They also are testing how the slow waves behave during disease.
Musicians who learn a new melody demonstrate enhanced skill after a night’s sleep
A new study that examined how the brain learns and retains motor skills provides insight into musical skill.
Performance of a musical task improved among pianists whose practice of a new melody was followed by a night of sleep, says researcher Sarah E. Allen, Southern Methodist University, Dallas.
The study is among the first to look at whether sleep enhances the learning process for musicians practicing a new piano melody.
The study found, however, that when two similar melodies were practiced one after the other, followed by sleep, any gains in speed and accuracy achieved during practice diminished overnight, said Allen, an assistant professor of music education in SMU’s Meadows School of the Arts.
“The goal is to understand how the brain decides what to keep, what to discard, what to enhance, because our brains are receiving such a rich data stream and we don’t have room for everything,” Allen said. “I was fascinated to study this because as musicians we practice melodies in juxtaposition with one another all the time.”
Surprisingly, in a third result the study found that when two similar musical pieces were practiced one after the other, followed by practice of the first melody again, a night’s sleep enhanced pianists’ skills on the first melody, she said.
“The really unexpected result that I found was that for those subjects who learned the two melodies, if before they left practice they played the first melody again, it seemed to reactivate that memory so that they did improve overnight. Replaying it seemed to counteract the interference of learning a second melody.”
The study adds to a body of research in recent decades that has found the brain keeps processing the learning of a new motor skill even after active training has stopped. That’s also the case during sleep.
The findings may in the future guide the teaching of music, Allen said.
“In any task we want to maximize our time and our effort. This research can ultimately help us practice in an advantageous way and teach in an advantageous way,” Allen said. “There could be pedagogical benefits for the order in which you practice things, but it’s really too early to say. We want to research this further.”
The study, “Memory stabilization and enhancement following music practice,” will be published in the journal Psychology of Music.
New study builds on earlier brain research in rats and humans
Researchers in the field of procedural memory consolidation have systematically examined the process in both rats and humans.
Studies have found that after practice of a motor skill, such as running a maze or completing a handwriting task, the areas of the brain activated during practice continue to be active for about four to six hours afterward. Activation occurs whether a subject is, for example, eating, resting, shopping or watching TV, Allen said.
Also, researchers have found that the area of the brain activated during practice of the skill is activated again during sleep, she said, essentially recalling the skill and enhancing and reinforcing it. For motor skills such as finger-tapping a sequence, research found that performance tends to be 10 percent to 13 percent more efficient after sleep, with fewer errors.
“There are two phases of memory consolidation. We refer to the four to six hours after training as stabilization. We refer to the phase during sleep as enhancement,” Allen said. “We know that sleep seems to play a very important role. It makes memories a more permanent, less fragile part of the brain.”
Allen’s finding with musicians that practicing a second melody interfered with retaining the first melody is consistent with a growing number of similar research studies that have found learning a second motor skill task interferes with enhancement of the first task.
Impact of sleep on learning for musicians
For Allen’s study, 60 undergraduate and graduate music majors participated in the research.
Divided into four groups, each musician practiced either one or both melodies during evening sessions, then returned the next day after sleep to be tested on their performance of the target melody.
The subjects learned the melodies on a Roland digital piano, practicing with their left hand during 12 30-second practice blocks separated by 30-second rest intervals. Software written for the experiment made it possible to digitally recorde musical instrument data from the performances. The number of correct key presses per 30-second block reflected speed and accuracy.
Musicians who learned a single melody showed performance gains on the test the next day.
Those who learned a second melody immediately after learning the target melody didn’t get any overnight enhancement in the first melody.
Those who learned two melodies, but practiced the first one again before going home to sleep, showed overnight enhancement when tested on the first melody.
“This was the most surprising finding, and perhaps the most important,” Allen reported in the Psychology of Music. “The brief test of melody A following the learning of melody B at the end of the evening training session seems to have reactivated the memory of melody A in a way that inhibited the interfering effects of learning melody B that were observed in the AB-sleep-A group.”— Margaret Allen
Reactivating memories during sleep
Why do some memories last a lifetime while others disappear quickly?
(Image: Tim Vernon, LTH NHS TRUST/SCIENCE PHOTO LIBRARY)
A new study suggests that memories rehearsed, during either sleep or waking, can have an impact on memory consolidation and on what is remembered later.
The new Northwestern University study shows that when the information that makes up a memory has a high value (associated with, for example, making more money), the memory is more likely to be rehearsed and consolidated during sleep and, thus, be remembered later.
Also, through the use of a direct manipulation of sleep, the research demonstrated a way to encourage the reactivation of low-value memories so they too were remembered later.
Delphine Oudiette, a postdoctoral fellow in the department of psychology at Northwestern and lead author of the study, designed the experiment to study how participants remembered locations of objects on a computer screen. A value assigned to each object informed participants how much money they could make if they remembered it later on the test.
"The pay-off was much higher for some of the objects than for others," explained Ken Paller, professor of psychology at Northwestern and co-author of the study. "In other words, we manipulated the value of the memories — some were valuable memories and others not so much, just as the things we experience each day vary in the extent to which we’d like to be able to remember them later."
When each object was shown, it was accompanied by a characteristic sound. For example, a tea kettle would appear with a whistling sound. During both states of wakefulness and sleep, some of the sounds were played alone, quite softly, essentially reminding participants of the low-value items.
Participants remembered the low-value associations better when the sound presentations occurred during sleep.
"We think that what’s happening during sleep is basically the reactivation of that information," Oudiette said. "We can provoke the reactivation by presenting those sounds, therefore energizing the low-value memories so they get stored better."
The research poses provocative implications about the role memory reactivation during sleep could play in improving memory storage,” said Paller, director of the Cognitive Neuroscience Program at Northwestern. “Whatever makes you rehearse during sleep is going to determine what you remember later, and conversely, what you’re going to forget.”
Many memories that are stored during the day are not remembered.
"We think one of the reasons for that is that we have to rehearse memories in order to keep them. When you practice and rehearse, you increase the likelihood of later remembering," Oudiette said. "And a lot of our rehearsal happens when we don’t even realize it — while we’re asleep."
Paller said selectivity of memory consolidation is not well understood. Most efforts in memory research have focused on what happens when you first form a memory and on what happens when you retrieve a memory.
"The in-between time is what we want to learn more about, because a fascinating aspect of memory storage is that it is not static," Paller said. "Memories in our brain are changing all of the time. Sometimes you improve memory storage by rehearsing all the details, so maybe later you remember better — or maybe worse if you’ve embellished too much.
"The fact that this critical memory reactivation transpires during sleep has mostly been hidden from us, from humanity, because we don’t realize so much of what’s happening while we’re asleep," he said.
(Source: eurekalert.org)
Sound stimulation during sleep can enhance memory
Slow oscillations in brain activity, which occur during so-called slow-wave sleep, are critical for retaining memories. Researchers reporting online April 11 in the Cell Press journal Neuron have found that playing sounds synchronized to the rhythm of the slow brain oscillations of people who are sleeping enhances these oscillations and boosts their memory. This demonstrates an easy and noninvasive way to influence human brain activity to improve sleep and enhance memory.
"The beauty lies in the simplicity to apply auditory stimulation at low intensities—an approach that is both practical and ethical, if compared for example with electrical stimulation—and therefore portrays a straightforward tool for clinical settings to enhance sleep rhythms," says coauthor Dr. Jan Born, of the University of Tübingen, in Germany.
Dr. Born and his colleagues conducted their tests on 11 individuals on different nights, during which they were exposed to sound stimulations or to sham stimulations. When the volunteers were exposed to stimulating sounds that were in sync with the brain’s slow oscillation rhythm, they were better able to remember word associations they had learned the evening before. Stimulation out of phase with the brain’s slow oscillation rhythm was ineffective.
"Importantly, the sound stimulation is effective only when the sounds occur in synchrony with the ongoing slow oscillation rhythm during deep sleep. We presented the acoustic stimuli whenever a slow oscillation "up state" was upcoming, and in this way we were able to strengthen the slow oscillation, showing higher amplitude and occurring for longer periods," explains Dr. Born.
The researchers suspect that this approach might also be used more generally to improve sleep. “Moreover, it might be even used to enhance other brain rhythms with obvious functional significance—like rhythms that occur during wakefulness and are involved in the regulation of attention,” says Dr. Born.