Both limited, excess sleep may raise diabetes risk in men Study is the first to show opposite effects of lost sleep in healthy men, women
June 29, 2016
Science Daily/The Endocrine Society
Men who sleep either fewer or more hours than average may face a greater risk of developing diabetes, according to a new study.
More than 29 million people nationwide have diabetes, according to the Endocrine Society's Endocrine Facts and Figures Report. During the last 50 years, the average self-reported sleep duration for individuals has decreased by 1.5 to 2 hours, according to the study's senior author, Femke Rutters, PhD, of the VU Medical Centre in Amsterdam, The Netherlands. The prevalence of diabetes has doubled in the same time period.
"In a group of nearly 800 healthy people, we observed sex-specific relationships between sleep duration and glucose metabolism," said Rutters. "In men, sleeping too much or too little was related to less responsiveness of the cells in the body to insulin, reducing glucose uptake and thus increasing the risk of developing diabetes in the future. In women, no such association was observed."
The cross-sectional study examined the sleep duration and diabetes risk factors in 788 people. The researchers analyzed a subset of participants in the European Relationship between Insulin Sensitivity and Cardiovascular Disease (EGIR-RISC) study, who were healthy adults ranging in age from 30 to 60 years old. Study participants were recruited from 19 study centers in 14 European countries.
Researchers measured the participants' sleep and physical activity using a single-axis accelerometer, a device to track movement. To assess the risk for diabetes, researchers used a device called a hyperinsulinemic-euglycemic clamp to measure how effectively the body used the hormone insulin, which processes sugar in the bloodstream.
The study found that men who slept the least and the most were more likely to have an impaired ability to process sugar compared to men who slept an average amount, about seven hours. The men at either end of the spectrum had higher blood sugar levels than men who got the average amount of sleep.
Women who slept less or more than average, however, were more responsive to the hormone insulin than women who slept the average amount. They also had enhanced function of beta cells -- the cells in the pancreas that produce the hormone insulin. This suggests lost sleep may not put women at increased risk of developing diabetes.
The study is the first to show opposite effects of lost sleep on diabetes risk in men and women. The authors theorized this may be a result of the study population being made up of healthy individuals, rather than those at risk of developing diabetes. The researchers also measured insulin sensitivity and sleep with more sensitive devices than past studies.
"Even when you are healthy, sleeping too much or too little can have detrimental effects on your health," Rutters said. "This research shows how important sleep is to a key aspect of health -- glucose metabolism."
https://www.sciencedaily.com/releases/2016/06/160629135234.htm
Poor sleep health could contribute to inflammatory disease
July 6, 2016
Science Daily/Elsevier
Sleep disturbances and long sleep duration are associated with increases in markers of inflammation, a new meta-analysis reports. Common sleep disturbances, such as insomnia, have been associated with increased risk of inflammatory disease and mortality.
"It is important to highlight that both too much and too little sleep appears to be associated with inflammation, a process that contributes to depression as well as many medical illnesses," said Dr. John Krystal, Editor of Biological Psychiatry.
Insufficient sleep is considered a public health epidemic by the Centers for Disease Control and Prevention. Common sleep disturbances, such as insomnia, have been associated with increased risk of inflammatory disease and mortality.
Substances that increase in response to inflammation and circulate in the blood stream, such as C-reactive protein (CRP) and interleukin-6 (IL-6), predict adverse health conditions including cardiovascular events, hypertension, and type 2 diabetes. Many studies have investigated the mechanism behind the association between sleep health and immunity, but variations between studies have made it difficult to understand the effects.
In a recent article, Michael Irwin, Richard Olmstead and Judith Carroll, all of the Cousins Center for Psychoneuroimmunology, UCLA Semel Institute for Neuroscience, University of California, Los Angeles, systematically reviewed existing studies for associations between sleep and inflammatory markers. The meta-analysis examined 72 different articles, which included over 50,000 participants from population-based and clinical studies. The researchers looked at CRP, IL-6, and tumor necrosis factor α (TNFα) as indicators of inflammation.
People with a normal sleep duration get 7-8 hours of shut-eye per night. The analysis showed that sleep disturbance (poor sleep quality or complaints of insomnia) and long sleep duration (more than 8 hours) were associated with increased levels of CRP and IL-6. Shorter sleep duration was associated with increased levels of CRP. No associations were found with TNFα.
According to Irwin, sleep disturbance or insomnia should be regarded as behavioral risk factors for inflammation, similar to the adverse effects of high fat diet or sedentary behavior. Treatments targeting sleep behavior could be a strategy for reversing the inflammation and reducing risk of inflammatory illnesses.
"Together with diet and physical activity, sleep health represents a third component in the promotion of health-span," said Irwin.
https://www.sciencedaily.com/releases/2016/07/160706091735.htm
East-west asymmetry of jet lag recovery due to oscillation of brain cells
July 12, 2016
Science Daily/American Institute of Physics
Travelers frequently report experiencing a significantly slower jet lag recovery after an eastward vs. westward flight. While some are quick to dismiss this complaint as being 'all in their head,' new research suggests it may be caused by the oscillation of a certain type of brain cells.
https://images.sciencedaily.com/2016/07/160712115332_1_540x360.jpg
Researchers explored the east-west asymmetry of jet lag recovery.
Credit: © Maxisport / Fotolia
Circadian rhythms, which govern jet lag recovery, are controlled by the synchronization of many neuronal oscillators within the brain. Brain cells within the hypothalamus -- the region of the brain that governs circadian rhythms -- undergo daily cycles of activity.
But after a rapid time zone shift, the brain's oscillatory circadian pacemaker cells are incapable of instantly adjusting to a rhythm appropriate to the new time zone.
So a team of University of Maryland researchers decided to explore whether the east-west asymmetry of jet lag could be understood via mathematical models of these oscillations of cells within the brain, and made some interesting discoveries about the dynamics involved, which they report in the journal Chaos, from AIP Publishing.
Akin to cars racing around a circular track, some of the brain's "circadian pacemaker cells" could complete the circuit faster on their own than others. But due to their mutual interactions sharing the track, these cells tend to form a traffic clump and travel around the track as a group.
"In the absence of a controlling influence, say 'a man with a yellow flag,' the clump of cells completes the circuit within a period of time that may not correspond exactly to one day," explained Michelle Girvan, an associate professor of physics at the University of Maryland's Institute for Physical Science and Technology.
Studies have shown that without daily variations of sunlight acting as that "man with the yellow flag," or traffic controller, the brain's circadian pacemaker cells complete their cycle in a time slightly longer than a day.
"Our mathematical model is based on this type of picture," Girvan said. "We start by explicitly modeling the dynamics of a large number of cells, and then use a novel method for simplifying this very large system to a single equation that can be easily analyzed."
What did they discover? While an average person's natural circadian rhythm is believed to slightly exceed 24 hours, the team's model indicated that this small amount of time -- on the order of 30 minutes -- is significant and can explain the rather large east-west asymmetry for jet lag recovery, which can equate to days when traveling across several times zones.
Their model also explains how individuals can experience a differing severity in response to rapid cross-time-zone travel. Since the neuronal oscillator cells of different individuals may have different properties, in the absence of regulation by the diurnal pattern of sunlight, "some people may have a natural circadian rhythm with a period of 24.5 hours, while others may have longer or shorter natural rhythms," Girvan elaborated. "Our model suggests that the difference between a person's natural period and 24 hours controls how they experience jet lag."
The team hopes that the mechanistic insights provided by their simplified model "can serve as a guide for developing more in-depth qualitative approaches, as well as strategies to combat circadian rhythm disruptions due to rapid cross-time-zone travel, shift work, or blindness," Girvan said.
https://www.sciencedaily.com/releases/2016/07/160712115332.htm
Is artificial lighting making us sick? New evidence in mice
July 14, 2016
Science Daily/Cell Press
Along with eating right and exercising, people should consider adding another healthy habit to their list: turning out the lights. That's according to a new study showing many negative health consequences for mice kept under conditions of constant light for a period of months.
https://images.sciencedaily.com/2016/07/160714134753_1_540x360.jpg
New findings suggest that more care should be taken in considering the amount of light exposure people get.
Credit: © meepoohyaphoto / Fotolia
"Our study shows that the environmental light-dark cycle is important for health," says Johanna Meijer of Leiden University Medical Center in the Netherlands. "We showed that the absence of environmental rhythms leads to severe disruption of a wide variety of health parameters."
Those parameters included pro-inflammatory activation of the immune system, muscle loss, and early signs of osteoporosis. The researchers say that the observed physiological changes were all indicative of "frailty" as is typically seen in people or animals as they age. But there was some more encouraging news, too.
"The good news is that we subsequently showed that these negative effects on health are reversible when the environmental light-dark cycle is restored," Meijer says.
To investigate the relationship between a loss of the light-dark cycle and disease, Meijer and colleagues, including Eliane Lucassen, exposed mice to light around the clock for 24 weeks and measured several major health parameters. Studies of the animals' brain activity showed that the constant light exposure reduced the normal rhythmic patterns in the brain's central circadian pacemaker of the suprachiasmatic nuclei (SCN) by 70 percent.
Strikingly, the disruption to normal light and dark patterns and the circadian rhythm led to a reduction in the animals' skeletal muscle function as measured in standard tests of strength. Their bones showed signs of deterioration, and the animals entered a pro-inflammatory state normally observed only in the presence of pathogens or other harmful stimuli. After the mice were returned to a standard light-dark cycle for 2 weeks, the SCN neurons rapidly recovered their normal rhythm, and the animals' health problems were reversed.
The findings suggest that more care should be taken in considering the amount of light exposure people get, particularly those who are aging or otherwise vulnerable. That's important given that 75 percent of the world's population is exposed to light during the night. Constant light exposure is very common in nursing homes and intensive care units, and many people also work into the night.
"We used to think of light and darkness as harmless or neutral stimuli with respect to health," Meijer says. "We now realize this is not the case based on accumulating studies from laboratories all over the world, all pointing in the same direction. Possibly this is not surprising as life evolved under the constant pressure of the light-dark cycle. We seem to be optimized to live under these cycles, and the other side of the coin is that we are now affected by a lack of such cycles."
The bottom line, according to the researchers is "light exposure matters."
They say they now plan to perform more in-depth analysis of the influence of distorted light-dark cycles on the immune system. They'd also like to investigate possible health benefits to patients exposed to more normal conditions of light and dark.
https://www.sciencedaily.com/releases/2016/07/160714134753.htm
New theory explains how beta waves arise in the brain
July 25, 2016
Science Daily/Brown University
A team of neuroscientists proposes a new theory -- backed by data from people, animal models and computational simulation -- to explain how beta waves emerge in the brain.
https://images.sciencedaily.com/2016/07/160725192354_1_540x360.jpg
Jones led a team that has posited a new theory of how beta rhythms arise in the brain, backed by evidence from humans, animal models and computer simulation.
Credit: Brown University
Beta rhythms, or waves of brain activity with an approximately 20 Hz frequency, accompany vital fundamental behaviors such as attention, sensation and motion and are associated with some disorders such as Parkinson's disease. Scientists have debated how the spontaneous waves emerge, and they have not yet determined whether the waves are just a byproduct of activity, or play a causal role in brain functions. Now in a new paper led by Brown University neuroscientists, they have a specific new mechanistic explanation of beta waves to consider.
The new theory, presented in the Proceedings of the National Academy of Sciences, is the product of several lines of evidence: external brainwave readings from human subjects, sophisticated computational simulations and detailed electrical recordings from two mammalian model organisms.
"A first step to understanding beta's causal role in behavior or pathology, and how to manipulate it for optimal function, is to understand where it comes from at the cellular and circuit level," said corresponding author Stephanie Jones, research associate professor of neuroscience at Brown University. "Our study combined several techniques to address this question and proposed a novel mechanism for spontaneous neocortical beta. This discovery suggests several possible mechanisms through which beta may impact function."
Making waves
The team started by using external magnetoencephalography (MEG) sensors to observe beta waves in the human somatosensory cortex, which processes sense of touch, and the inferior frontal cortex, which is associated with higher cognition.
They closely analyzed the beta waves, finding they lasted at most a mere 150 milliseconds and had a characteristic wave shape, featuring a large, steep valley in the middle of the wave.
The question from there was what neural activity in the cortex could produce such waves. The team sought to recreate the waves using a computer model of a cortical circuitry, made up of a multilayered cortical column that contained multiple cell types across different layers. Importantly, the model was designed to include a cell type called pyramidal neurons, whose activity is thought to dominate the human MEG recordings.
They found that they could closely replicate the shape of the beta waves in the model by delivering two kinds of excitatory synaptic stimulation to distinct layers in the cortical columns of cells: one that was weak and broad in duration to the lower layers, contacting spiny dendrites on the pyramidal neurons close to the cell body; and another that was stronger and briefer, lasting 50 milliseconds (i.e., one beta period), to the upper layers, contacting dendrites farther away from the cell body. The strong distal drive created the valley in the waveform that determined the beta frequency.
Meanwhile they tried to model other hypotheses about how beta waves emerge, but found those unsuccessful.
With a model of what to look for, the team then tested it by looking for a real biological correlate of it in two animal models. The team analyzed measurements in the cortex of mice and rhesus macaques and found direct confirmation that this kind of stimulation and response occurred across the cortical layers in the animal models.
"The ultimate test of the model predictions is to record the electrical signals inside the brain," Jones said. "These recordings supported our model predictions."
Beta in the brain
Neither the computer models nor the measurements traced the source of the excitatory synaptic stimulations that drive the pyramidal neurons to produce the beta waves, but Jones and her co-authors posit that they likely come from the thalamus, deeper in the brain. Projections from the thalamus happen to be in exactly the right places needed to deliver signals to the right positions on the dendrites of pyramidal neurons in the cortex. The thalamus is also known to send out bursts of activity that last 50 milliseconds, as predicted by their theory.
With a new biophysical theory of how the waves emerge, the researchers hope the field can now investigate whether beta rhythms affect or merely reflect behavior and disease. Jones's team in collaboration with Professor of neuroscience Christopher Moore at Brown is now testing predictions from the theory that beta may decrease sensory or motor information processing functions in the brain. New hypotheses are that the inputs that create beta may also stimulate inhibitory neurons in the top layers of the cortex, or that they may may saturate the activity of the pyramidal neurons, thereby reducing their ability to process information; or that the thalamic bursts that give rise to beta occupy the thalamus to the point where it doesn't pass information along to the cortex.
Figuring this out could lead to new therapies based on manipulating beta, Jones said.
"An active and growing field of neuroscience research is trying to manipulate brain rhythms for optimal function with stimulation techniques," she said. "We hope that our novel finding on the neural origin of beta will help guide research to manipulate beta, and possibly other rhythms, for improved function in sensorimotor pathologies."
https://www.sciencedaily.com/releases/2016/07/160725192354.htm
No dream: Electric brain stimulation during sleep can boost memory
July 28, 2016
Science Daily/University of North Carolina Health Care
For the first time, scientists report using transcranial alternating current stimulation, or tACS, to target a specific kind of brain activity during sleep and strengthen memory in healthy people.
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Could brain stimulation during sleep boost memory?
Credit: © elnariz / Fotolia
When you sleep, your brain is busy storing and consolidating things you learned that day, stuff you'll need in your memory toolkit tomorrow, next week, or next year. For many people, especially those with neurological conditions, memory impairment can be a debilitating symptom that affects every-day life in profound ways. For the first time, UNC School of Medicine scientists report using transcranial alternating current stimulation, or tACS, to target a specific kind of brain activity during sleep and strengthen memory in healthy people.
The findings, published in the journal Current Biology, offer a non-invasive method to potentially help millions of people with conditions such as autism, Alzheimer's disease, schizophrenia, and major depressive disorder.
For years, researchers have recorded electrical brain activity that oscillates or alternates during sleep; they present as waves on an electroencephalogram (EEG). These waves are called sleep spindles, and scientists have suspected their involvement in cataloging and storing memories as we sleep.
"But we didn't know if sleep spindles enable or even cause memories to be stored and consolidated," said senior author Flavio Frohlich, PhD, assistant professor of psychiatry and member of the UNC Neuroscience Center. "They could've been merely byproducts of other brain processes that enabled what we learn to be stored as a memory. But our study shows that, indeed, the spindles are crucial for the process of creating memories we need for every-day life. And we can target them to enhance memory."
This marks the first time a research group has reported selectively targeting sleep spindles without also increasing other natural electrical brain activity during sleep. This has never been accomplished with tDCS -- transcranial direct current stimulation -- the much more popular cousin of tACS in which a constant stream of weak electrical current is applied to the scalp.
During Frohlich's study, 16 male participants underwent a screening night of sleep before completing two nights of sleep for the study.
Before going to sleep each night, all participants performed two common memory exercises -- associative word-pairing tests and motor sequence tapping tasks, which involved repeatedly finger-tapping a specific sequence. During both study nights, each participant had electrodes placed at specific spots on their scalps. During sleep one of the nights, each person received tACS -- an alternating current of weak electricity synchronized with the brain's natural sleep spindles. During sleep the other night, each person received sham stimulation as placebo.
Each morning, researchers had participants perform the same standard memory tests. Frohlich's team found no improvement in test scores for associative word-pairing but a significant improvement in the motor tasks when comparing the results between the stimulation and placebo night.
"This demonstrated a direct causal link between the electric activity pattern of sleep spindles and the process of motor memory consolidation." Frohlich said.
Caroline Lustenberger, PhD, first author and postdoctoral fellow in the Frohlich lab, said, "We're excited about this because we know sleep spindles, along with memory formation, are impaired in a number of disorders, such as schizophrenia and Alzheimer's. We hope that targeting these sleep spindles could be a new type of treatment for memory impairment and cognitive deficits."
Frohlich said, "The next step is to try the same intervention, the same type of non-invasive brain stimulation, in patients that have known deficits in these spindle activity patterns."
Frohlich's team previously used tACS to target the brain's natural alpha oscillations to boost creativity. This was a proof of concept. It showed it was possible to target these particular brain waves, which are prominent as we create ideas, daydream, or meditate. These waves are impaired in people with neurological and psychiatric illnesses, including depression.
https://www.sciencedaily.com/releases/2016/07/160728143247.htm
Brain areas altered during hypnotic trances identified
July 28, 2016
Science Daily/Stanford University Medical Center
By scanning the brains of subjects while they were hypnotized, researchers were able to see the neural changes associated with hypnosis.
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Stanford researchers found changes in three areas of the brain that occur when people are hypnotized. (Stock image)
Credit: © WavebreakmediaMicro / Fotolia
Your eyelids are getting heavy, your arms are going limp and you feel like you're floating through space. The power of hypnosis to alter your mind and body like this is all thanks to changes in a few specific areas of the brain, researchers at the Stanford University School of Medicine have discovered.
The scientists scanned the brains of 57 people during guided hypnosis sessions similar to those that might be used clinically to treat anxiety, pain or trauma. Distinct sections of the brain have altered activity and connectivity while someone is hypnotized, they report in a study that will be published online July 28 in Cerebral Cortex.
"Now that we know which brain regions are involved, we may be able to use this knowledge to alter someone's capacity to be hypnotized or the effectiveness of hypnosis for problems like pain control," said the study's senior author, David Spiegel, MD, professor and associate chair of psychiatry and behavioral sciences.
A serious science
For some people, hypnosis is associated with loss of control or stage tricks. But doctors like Spiegel know it to be a serious science, revealing the brain's ability to heal medical and psychiatric conditions.
"Hypnosis is the oldest Western form of psychotherapy, but it's been tarred with the brush of dangling watches and purple capes," said Spiegel, who holds the Jack, Samuel and Lulu Willson Professorship in Medicine. "In fact, it's a very powerful means of changing the way we use our minds to control perception and our bodies."
Despite a growing appreciation of the clinical potential of hypnosis, though, little is known about how it works at a physiological level. While researchers have previously scanned the brains of people undergoing hypnosis, those studies have been designed to pinpoint the effects of hypnosis on pain, vision and other forms of perception, and not the state of hypnosis itself.
"There had not been any studies in which the goal was to simply ask what's going on in the brain when you're hypnotized," said Spiegel.
Finding the most susceptible
To study hypnosis itself, researchers first had to find people who could or couldn't be hypnotized. Only about 10 percent of the population is generally categorized as "highly hypnotizable," while others are less able to enter the trancelike state of hypnosis. Spiegel and his colleagues screened 545 healthy participants and found 36 people who consistently scored high on tests of hypnotizability, as well as 21 control subjects who scored on the extreme low end of the scales.
Then, they observed the brains of those 57 participants using functional magnetic resonance imaging, which measures brain activity by detecting changes in blood flow. Each person was scanned under four different conditions -- while resting, while recalling a memory and during two different hypnosis sessions.
"It was important to have the people who aren't able to be hypnotized as controls," said Spiegel. "Otherwise, you might see things happening in the brains of those being hypnotized but you wouldn't be sure whether it was associated with hypnosis or not."
Brain activity and connectivity
Spiegel and his colleagues discovered three hallmarks of the brain under hypnosis. Each change was seen only in the highly hypnotizable group and only while they were undergoing hypnosis.
First, they saw a decrease in activity in an area called the dorsal anterior cingulate, part of the brain's salience network. "In hypnosis, you're so absorbed that you're not worrying about anything else," Spiegel explained.
Secondly, they saw an increase in connections between two other areas of the brain -- the dorsolateral prefrontal cortex and the insula. He described this as a brain-body connection that helps the brain process and control what's going on in the body.
Finally, Spiegel's team also observed reduced connections between the dorsolateral prefrontal cortex and the default mode network, which includes the medial prefrontal and the posterior cingulate cortex. This decrease in functional connectivity likely represents a disconnect between someone's actions and their awareness of their actions, Spiegel said. "When you're really engaged in something, you don't really think about doing it -- you just do it," he said. During hypnosis, this kind of disassociation between action and reflection allows the person to engage in activities either suggested by a clinician or self-suggested without devoting mental resources to being self-conscious about the activity.
Treating pain and anxiety without pills
In patients who can be easily hypnotized, hypnosis sessions have been shown to be effective in lessening chronic pain, the pain of childbirth and other medical procedures; treating smoking addiction and post-traumatic stress disorder; and easing anxiety or phobias. The new findings about how hypnosis affects the brain might pave the way toward developing treatments for the rest of the population -- those who aren't naturally as susceptible to hypnosis.
"We're certainly interested in the idea that you can change people's ability to be hypnotized by stimulating specific areas of the brain," said Spiegel.
A treatment that combines brain stimulation with hypnosis could improve the known analgesic effects of hypnosis and potentially replace addictive and side-effect-laden painkillers and anti-anxiety drugs, he said. More research, however, is needed before such a therapy could be implemented.
https://www.sciencedaily.com/releases/2016/07/160728100926.htm
Insomnia? Oversleeping? Both may increase your risk of stroke
August 3, 2016
Science Daily/American Academy of Neurology
There is growing evidence that sleep disorders like insomnia and sleep apnea are related to stroke risk and recovery from stroke, according to a recent literature review.
Based on the review, the authors recommend that people who have had a stroke or a mini-stroke, called a transient ischemic attack, be screened for sleep disorders.
"Although sleep disorders are common after a stroke, very few stroke patients are tested for them," said study author Dirk M. Hermann, MD, of University Hospital Essen in Essen, Germany. "The results of our review show that should change, as people with sleep disorders may be more likely to have another stroke or other negative outcomes than people without sleep problems, such as having to go to a nursing home after leaving the hospital."
The researchers also recommend that sleep apnea be treated with a continuous positive airway pressure machine (CPAP), based on evidence that shows that its use can improve outcomes after stroke.
For the literature review, the researchers examined dozens of studies that looked at the link between sleep disturbances and stroke. They then combined the data of multiple studies in a meta-analysis.
Sleep disorders generally fall into two categories: sleep breathing problems and sleep-wake disorders. Sleep breathing problems like sleep apnea disrupt breathing while asleep. Sleep-wake disorders like insomnia and restless leg syndrome affect the amount of time spent asleep.
The review found evidence linking sleep breathing problems with stroke risk and recovery. Sleep-wake disorders may increase stroke risk and harm recovery, although there is less evidence to prove so.
Due to this lack of evidence and to possible side effects, the researchers are cautious to recommend treatment of sleep-wake disorders with drugs.
https://www.sciencedaily.com/releases/2016/08/160803214246.htm
Dreaming also occurs during non rapid eye movement sleep
August 9, 2016
Science Daily/Aalto University
Measurements demonstrated that the brain activity of people who dream during NREM sleep, compared to people who do not dream in NREM sleep, is closer to brain activity of awake people.
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Dr. Gosseries and Dr. Nieminen are preparing a subject (Bjørn Erik Juel) for the experiment.
Credit: Johan Frederik Storm
Researchers from Aalto University and the University of Wisconsin utilised a TMS-EEG device, which combines transcranial magnetic stimulation and EEG, to examine how the brain activity of people in the restful non-rapid eye movement (NREM) sleep is affected by whether they dream or do not dream.
When the NREM sleep of subjects had lasted at least three minutes, researchers gave magnetic pulses that induced a weak electric field and activated neurons. After a series of pulses, the subject was woken with an alarm sound, and they were then asked whether they had dreamed and to describe the content of the dream.
'It is traditionally thought that dreaming occurs only in REM sleep. However, as also our study demonstrates, subjects woken from NREM sleep are also able to give accounts of their dreams in more than half of cases,' Post-doctoral Researcher Jaakko Nieminen from Aalto University explains.
'EEG showed that the deterministic brain activity produced by magnetic pulses was notably shorter in people who did not dream, i.e. were unconscious, than in people who had dreamt. We also observed that the longer the story about the dream, the more the subject's EEG resembled that measured from people who were awake,' Dr Nieminen explains.
Assessment of consciousness may help in treatment of brain injury patients
Dr Nieminen performed the measurements with his research colleague Olivia Gosseries at the University of Wisconsin-Madison Center for Sleep and Consciousness, which is headed by Giulio Tononi. The measurements were carried out during a period of over 40 nights and a total of 11 subjects participated. Due to sleeping difficulties and other challenges, reliable measurements could only be acquired from six subjects. During the night, subjects were woken a maximum of 16 times.
'Consciousness in different physiological states (e.g. during wakefulness, sleep, anesthesia and vegetative state) has previously been researched with TMS-EEG measurements. We wanted to eliminate all other differences related to the different states as thoroughly as possible, and for this reason we focused on the narrow physiological state of NREM sleep,' Dr Nieminen notes.
Transcranial magnetic stimulation is already utilised in such things as the treatment of depression and pain. According to Dr Nieminen, in the future the precise data provided by TMS-EEG measurements on the state of consciousness may also help in the treatment of brain injury patients who are unable to communicate.
https://www.sciencedaily.com/releases/2016/08/160809121817.htm
Light, caffeine improve driver alertness
August 9, 2016
Science Daily/Queensland University of Technology
Bright light combined with caffeine can improve driving performance and alertness of chronically sleep deprived young drivers, according to a road safety study.
The use of smartphones and tablet computers during evening hours has previously been associated with sleep disturbances in humans. A new study from Uppsala University now shows that daytime light exposure may be a promising means to combat sleep disturbances associated with evening use of electronic devices. The findings are published in the scientific journal Sleep Medicine.
Dr Shamsi Shekari, from QUT's Centre for Accident Research & Road Safety -- Queensland (CARRS-Q) presented her findings at the 2016 International Conference on Traffic and Transport Psychology held in Australia this month.
CARRS-Q and Griffith University co-hosted the event which brought together international experts from across the globe to share the latest in road safety research with the aim of reducing road trauma.
As part of her PhD, Dr Shekari tested the novel and potentially effective use of bright light, using commercially available light glasses that emit a shortwave blue-green light, and caffeinated chewing gum on young drivers aged 18-25 in a driving simulator to see if it increased alertness during daytime driving.
"Light therapy is being used to adjust a person's circadian rhythm in shift workers and pilots and offers the potential to reduce sleepiness," she said.
"The study found there was a significant effect on driving performance, mostly when caffeine was used alone or combined with light.
"Drivers who were given just caffeine, or light and caffeine together had decreased side to side movement of the steering wheel and the vehicle, indicating better control of the vehicle and higher alertness.
"Drivers who were feeling some signs of sleepiness after sleep loss, felt less sleepy after receiving either light or caffeine, and even felt rather alert after receiving the combination of both."
Dr Shekari said the two-week study included monitoring sleep-wake patterns, with a normal eight hours of time in bed in the first week being reduced by to seven hours in the second week to produce chronic sleep deprivation in the participants.
"On the last three days participants took test sessions which involved recording their brain and heart activity, reaction times, assessment of their sleepiness and two 50km-long simulated drives each day," she said.
"To compare the effectiveness of the countermeasures, all participants were provided with inactive chewing gum and light in the first drive and randomised active chewing gum and light in the second drive."
Dr Shekari said driver sleepiness accounted for 20 per cent of all crashes in developed countries, and young drivers were at an increased risk of chronic sleep deprivation.
"This is due to later brain development and social factors such as friends, work patterns and increased use of drugs and alcohol, all of which impact on sleep," she said.
Dr Shekari said while her study had revealed promising results of the use of light and caffeine to improve driver alertness, more research was needed.
"CARRS-Q is now undertaking a study on the effect of sleep loss and caffeine on driving where we want to learn more specifically about the effect of daytime sleepiness and caffeine on driver performance," she said.
https://www.sciencedaily.com/releases/2016/08/160809122734.htm
Plenty of light during daytime reduces the effect of blue light screens on night sleep
August 10, 2016
Science Daily/Uppsala University
The use of smartphones and tablet computers during evening hours has previously been associated with sleep disturbances in humans. A new study now shows that daytime light exposure may be a promising means to combat sleep disturbances associated with evening use of electronic devices.
The use of blue light emitting devices during evening hours has been shown to interfere with sleep in humans. In a new study from Uppsala University involving 14 young females and males, neuroscientists Christian Benedict and Frida Rångtell sought to investigate the effects of evening reading on a tablet computer on sleep following daytime bright light exposure.
'Our main finding was that following daytime bright light exposure, evening use of a self-luminous tablet for two hours did not affect sleep in young healthy students', says Frida Rångtell, first author and PhD student at the Department of Neuroscience at Uppsala University.
'Our results could suggest that light exposure during the day, e.g. by means of outdoor activities or light interventions in offices, may help combat sleep disturbances associated with evening blue light stimulation. Even if not examined in our study, it must however be kept in mind that utilizing electronic devices for the sake of checking your work e-mails or social network accounts before snoozing may lead to sleep disturbances as a result of emotional arousal', says senior author Christian Benedict, associate professor at the Department of Neuroscience.
https://www.sciencedaily.com/releases/2016/08/160810104246.htm
No blue light, please, I'm tired: Light color determines sleepiness versus arousal in mice
August 15, 2016
Science Daily/PLOS
Light affects sleep. A study in mice shows that the actual color of light matters; blue light keeps mice awake longer while green light puts them to sleep easily.
Light shining into our eyes not only mediates vision but also has critical non-image-forming functions such as the regulation of circadian rhythm, which affects sleep and other physiological processes. As humans, light generally keeps us awake, and dark makes us sleepy. For mice, which are mostly nocturnal, light is a sleep-inducer. Previous studies in mice and humans have shown that non-image-forming light perception occurs in specific photosensitive cells in the eye and involves a light sensor called melanopsin. Mice without melanopsin show a delay in their response to fall asleep when exposed to light, pointing to a critical role for melanopsin in sleep regulation.
Stuart Peirson and Russell Foster, both from Oxford University, UK, alongside colleagues from Oxford and elsewhere, investigated this further by studying sleep induction in mice exposed to colored light, i.e., light of different wave lengths. Based on the physical properties of melanopsin, which is most sensitive to blue light, the researchers predicted that blue light would be the most potent sleep inducer.
To their surprise, that was not the case. Green light, it turns out, puts mice to sleep quickly, whereas blue light actually seems to stimulate the mice, though they did fall asleep eventually. Mice lacking melanopsin were oblivious to light color, demonstrating that the protein is directing the differential response.
Both green and blue light elevated levels of the stress hormone corticosterone in the blood of exposed mice compared with mice kept in the dark, the researchers found. Corticosterone levels in response to blue light, however, were higher than levels in mice exposed to green light. When the researchers gave the mice drugs that block the effects of corticosterone, they were able to mitigate the effects of blue light; drugged mice exposed to blue light went to sleep faster than control mice that had received placebos.
Citing previous results that exposure to blue light -- a predominant component of light emitted by computer and smart-phone screens -- promotes arousal and wakefulness in humans as well, the researchers suggest that "despite the differences between nocturnal and diurnal species, light may play a similar alerting role in mice as has been shown in humans." Overall, they say their work "shows the extent to which light affects our physiology and has important implications for the design and use of artificial light sources."
In the accompanying Primer, Patrice Bourgin, from the University of Strasbourg, France, and Jeffrey Hubbard from the University of Lausanne, Switzerland, say the study "reveals that the role of color [in controlling sleep and alertness] is far more important and complex than previously thought, and is a key parameter to take into account." The study's results, they say, "call for a greater understanding of melanopsin-based phototransduction and tell us that color wavelength is another aspect of environmental illumination that we should consider, in addition to photon density, duration of exposure and time of day, as we move forward in designing the lighting of the future, aiming to improve human health and well-being."
https://www.sciencedaily.com/releases/2016/08/160815185816.htm
When you don't feel valued in a relationship, sleep suffers
August 17, 2016
Science Daily/Society for Personality and Social Psychology
We spend up to one-third of our life asleep, but not everyone sleeps well. For couples, it turns out how well you think your partner understands and cares for you is linked to how well you sleep.
"Our findings show that individuals with responsive partners experience lower anxiety and arousal, which in turn improves their sleep quality," says lead author Dr. Emre Selçuk, a developmental and social psychologist at Middle East Technical University in Turkey.
One of the most important functions of sleep is to protect us against deteriorations in physical health. However, this protective function of sleep can only be realized when we have high quality uninterrupted sleep, known as restorative sleep.
Restorative sleep requires feelings of safety, security, protection and absence of threats. For humans, the strongest source of feelings of safety and security is responsive social partners -- whether parents in childhood or romantic partners in adulthood.
"Having responsive partners who would be available to protect and comfort us should things go wrong is the most effective way for us humans to reduce anxiety, tension, and arousal," says Selçuk.
The research supports findings from the past several years by an international collaboration of researchers including Emre Selçuk (Middle East Technical University, Turkey), Anthony Ong (Cornell University, US), Richard Slatcher and Sarah Stanton (Wayne State University, US), Gul Gunaydin (Bilkent University, Turkey), and David Almeida (Penn State, US).
Using data from the Midlife Development in the United States project, past projects from the researchers showed connections between partner responsiveness, physical health and psychological well-being over several years.
"Taken together, the corpus of evidence we obtained in recent years suggests that our best bet for a happier, healthier, and a longer life is having a responsive partner," says Selçuk.
https://www.sciencedaily.com/releases/2016/08/160817090618.htm
Disruptions to sleep patterns lead to an increased risk of suicides
August 24, 2016
Science Daily/Manchester University
The link between sleep problems and suicidal thoughts and behaviors is made starkly clear in new research.
In this study, conducted by researchers from the University's School of Health Sciences alongside the University of Oxford, 18 participants were interviewed about the role sleep problems have on suicidal tendencies.
Three inter-related pathways to suicidal thoughts were identified arising from sleep problems. The first was that being awake at night heightened the risks of suicidal thoughts and attempts, which in part was seen as a consequence of the lack of help or resources available at night.
Secondly, the research found that a prolonged failure to achieve a good night's sleep made life harder for respondents, adding to depression, as well as increasing negative thinking, attention difficulties and inactivity.
Finally, respondents said sleep acted as an alternative to suicide, providing an escape from their problems. However, the desire to use sleep as an avoidance tactic led to increased day time sleeping which in turn caused disturbed sleeping patterns -- reinforcing the first two pathways.
Donna Littlewood, lead author of the study, said the research has implications for service providers, such as health care specialist and social services.
"Our research underscores the importance of restoring healthy sleep in relation to coping with mental health problems, suicidal thoughts and behaviours.
"Additionally, night time service provision should be a key consideration within suicide prevention strategies, given that this study shows that those who are awake in the night are at an increased risk of suicide."
https://www.sciencedaily.com/releases/2016/08/160824111104.htm
'Morning people' self-sabotage less at night, night owls' less at sunrise
August 30, 2016
Science Daily/Indiana University
A study by psychological researchers shows that people are more likely to undermine their performance at stressful tasks when they're operating at 'peak capacity' based on their preferred time of the day.
The seemingly counterintuitive results, recently reported in the Journal of Experimental Social Psychology, are based on an investigation into the connection between people's circadian rhythm and risk of "self-handicapping," or self-sabotage. But rather than trying to protect against possible failure more at "off-peak" times, the study found, people actually engage in this behavior more at their peak times.
In other words, "morning people," who reported greater alertness at sunrise, self-handicapped more in the morning, and "night owls," who reported greater alertness at sunset, self-handicapped more in the evening.
Self-handicapping is defined by psychologists as when an individual seeks to protect their ego against potential failure in advance by creating circumstances -- real or imagined -- that harm their ability to carry out a stressful task. A classic example is failing to study or staying out too late the night before an important test or job interview.
The behavior also extends to mere claims of debilitating circumstances, such as imagined illness, fatigue or stress. Other studies have linked self-handicapping to other self-destructive behaviors, such as aggression, overeating and drug or alcohol addiction.
The study also found that people chronically prone to making excuses reported the same stress levels at "off-peak" hours as peers who do not engage in this behavior. Only at peak hours did these individuals report higher levels of stress as an excuse for poor performance.
"What this study tells us is that self-handicapping requires thought and planning," said Ed Hirt, professor in the IU Bloomington College of Arts and Sciences' Department of Psychological and Brain Sciences and an author on the study. "People who are feeling uncertain about themselves and start to fear that they might fail are more likely to identify potential excuses and self-handicap when they're at their peak than when they're not."
"When an individual's positive self-views are threatened, they may lash out against the source of the threat, compare themselves to others worse off than themselves, or engage in self-destructive actions, such as substance abuse," added Julie Eyink, a graduate student in Hirt's lab and lead author on the study. "Unfortunately, it's not uncommon to get caught in a negative spiral, in which self-handicapping leads to lower self-esteem and higher failure beliefs, which prompt more self-handicapping."
To conduct the study, IU researchers administered intelligent tests to 237 students (98 men and 139 women), half of whom were told that stress had been found to affect performance on the test and half of whom were told that stress should not affect the result.
The tests were randomly administered at 8 a.m. or 8 p.m. to volunteers who had been previously categorized as "night people" or "morning people" based upon a survey shown to accurately predict circadian rhythm. Study participants were also assessed for their tendency to self-sabotage through questions about their stress levels prior to the exam.
The tests and morning or night preference assessments were given two weeks apart, and participants were unaware that circadian rhythm would be a factor in the study. The individuals who administered the tests were unaware who had been labeled "morning people" or "night owls."
The results were that people who scored higher in terms of risk for self-sabotage reported greater stress levels at hours of peak performance.
A high or low tendency to self-sabotage did not make a difference at off-peak hours, however. Both groups reported the same stress levels at these times.
"The results seem counterintuitive, but what they really show is clear evidence that self-handicapping is a resource demanding strategy," said Eyink. "Only people who had their peak cognitive resources were able to engage in self-handicapping."
Based solely on the study, she said people who want to avoid self-sabotage might conclude they should engage in stressful tasks at off-peak times. But she also warns that such a strategy would require carrying out tasks at a time when a person lacks all the cognitive tools required to achieve top performance.
"Ultimately," she said, "I would advise that working to avoid self-handicapping -- through actions such as healthful practices, seeking help or counseling -- is the best strategy."
Other authors on the paper were Eric Galante and Kristin S. Hendrix, an undergraduate student and PhD student at IU Bloomington, respectively, at the time of the study.
https://www.sciencedaily.com/releases/2016/08/160830131200.htm
Adapting to stress: Understanding the neurobiology of resilience
September 2, 2016
Science Daily/Taylor & Francis
New research examines the way our bodies, specifically our brains, become “stress-resilient.” There is a significant variation in the way individuals react and respond to extreme stress and adversity—some individuals develop psychiatric conditions such as posttraumatic stress disorder or major depressive disorder—others recover from stressful experiences without displaying significant symptoms of psychological ill-health, demonstrating stress-resilience.
"Adapting to Stress: Understanding the Neurobiology of Resilience," an article recently published in Behavioral Medicine, examines the way our bodies, specifically our brains, become "stress-resilient." There is a significant variation in the way individuals react and respond to extreme stress and adversity -- some individuals develop psychiatric conditions such as posttraumatic stress disorder or major depressive disorder -- others recover from stressful experiences without displaying significant symptoms of psychological ill-health, demonstrating stress-resilience.
To understand why some individuals exhibit characteristics of a resilient profile, the interplay between neurochemical, genetic, and epigenetic processes over time needs to be explained. In this review, the authors examine the hormones, neuropeptides, neurotransmitters, and neural circuits associated with resilience and vulnerability to stress-related disorders.
About the importance of their article, the authors state: "In a period of international conflict as well as domestic pressures within the NHS, the study of stress and resilience has again become a prescient topic for both military and medical communities. The experience of extreme or prolonged stress does not necessarily result in mental health problems, which is an increasingly overlooked point and one of real significance to the field of psychopathology. Scientific evidence has consistently shown us that a high number of individuals are able to overcome stress and adversity and to continue on with productive lives. In this review, we summarize some of the latest findings underlying the neurobiology of resilience, which we hope will advance the understanding and treatment of stress-related psychiatric disorders."
https://www.sciencedaily.com/releases/2016/09/160902142232.htm
Brain circuit that drives sleep-wake states, sleep-preparation behavior is identified
September 5, 2016
Science Daily/Stanford University Medical Center
A brain circuit that's indispensable to the sleep-wake cycle has now been identified by researchers. This same circuit is also a key component of the reward system, an archipelago of interconnected brain clusters crucial to promoting behavior necessary for animals, including humans, to survive and reproduce.
It makes intuitive sense that the reward system, which motivates goal-directed behaviors such as fleeing from predators or looking for food, and our sleep-wake cycle would coordinate with one another at some point. You can't seek food in your sleep, unless you're an adept sleepwalker. Conversely, getting out of bed is a lot easier when you're excited about the day ahead of you.
But until this study, no precise anatomical location for this integration of the brain's reward and arousal systems has been pinpointed, said Luis de Lecea, PhD, professor of psychiatry and behavioral sciences.
The researchers' findings will be published online Sept. 5 in Nature Neuroscience. De Lecea is the senior author. The lead author is postdoctoral scholar Ada Eban-Rothschild, PhD.
"This has potential huge clinical relevance," de Lecea said. "Insomnia, a multibillion-dollar market for pharmaceutical companies, has traditionally been treated with drugs such as benzodiazepines that nonspecifically shut down the entire brain. Now we see the possibility of developing therapies that, by narrowly targeting this newly identified circuit, could induce much higher-quality sleep."
Some 25 to 30 percent of American adults are affected by sleep disturbances of one type or another, according to the National Institutes of Health. In addition, disruption of the sleep-wake rhythm typifies many different neuropsychiatric disorders and is understood to exacerbate them.
One of the first questions a psychiatrist asks a patient, said de Lecea, is, "How's your sleep?"
Similarity across vertebrates
The reward system's circuitry is similar in all vertebrates, from fish, frogs and falcons to fishermen and fashion models. A chemical called dopamine plays a crucial role in firing up this circuitry.
Neuroscientists know that a particular brain structure, the ventral tegmental area, or VTA, is the origin of numerous dopamine-secreting nerve fibers that run in discrete tracts to many different parts of the brain. A plurality of these fibers go to the nucleus accumbens, a forebrain structure particularly implicated in generating feelings of pleasure in anticipation of, or response to, obtaining a desired objective.
"Since many reward-circuit-activating drugs such as amphetamines that work by stimulating dopamine secretion also keep users awake, it's natural to ask if dopamine plays a key role in the sleep-wake cycle as well as in reward," Eban-Rothschild said. "But, in part due to existing technical limitations, earlier experimental literature has unearthed little evidence for the connection and, in fact, has suggested that this circuit probably wasn't so important."
For the new study, the investigators employed male laboratory mice bioengineered in several respects to enable the use of advanced technologies to remotely excite, suppress and monitor activity in the dopamine-secreting nerve cells from the mice's VTA. The researchers also measured the mice's overall brain activity and muscle tone to determine the mice's relative stages of asleep or arousal. They used video cameras to view the mice's behavior.
Observed in mice
Overall, activity in the dopamine-secreting nerve cells emanating from the VTA rose on waking and stayed elevated when mice were awake. Conversely, this activity ramped down when mice transitioned into sleep, remaining low while they slumbered. Activating this nerve-cell population was enough to rouse the animals from a sound sleep and keep them awake for long periods, even during a point in the mice's diurnal cycle when they'd ordinarily be bunking down. Control animals, whose VTA activity wasn't similarly jacked up, built little nests from pellets of materials placed in all the mice's cages and then promptly dropped off.
When instead the scientists suppressed activity in the same nerve-cell population during the typically active period of the mice's 24-hour cycle, the mice conked out, snoozing through the presence of surefire arousal triggers: delicious high-fat chow, a female or fear-inducing fox urine.
Mice in an unfamiliar cage ordinarily explore their new surroundings energetically. And indeed, VTA-suppressed mice stayed awake for the first 45 minutes of the hour they spent in a new cage. But Eban-Rothschild noticed something: They spent that waking time building nests.
"They were really careful about it," she noted. Once they were satisfied with what they'd built, they dozed off.
This wasn't just some stereotyped behavior guaranteed to emerge when VTA activity was inhibited, Eban-Rothschild added. "If we put the nest they'd already built in their usual cage into the novel cage, they climbed in and went right to sleep."
Control mice in the unfamiliar cage ran around, either ignoring the pellet of nesting materials placed inside or scattering those materials all over the cage.
Nest-making activities
Eban-Rothschild analyzed video footage of the animals' behavior in their novel environments, and correlated 1-second video segments with recorded brain activity during the corresponding time frame. She saw that actions directly connected to building nests were marked by reduced VTA activity, while actions that weren't were associated with higher levels of VTA activity.
"We knew stimulating the brain's dopamine-related circuitry would increase goal-directed behaviors such as food- and sex-seeking" said Eban-Rothschild. "But the new study shows that at least one complex behavior is induced not by stimulating, but by inhibiting, this very circuit. Interestingly, this behavior -- nest building -- is essential to a mouse's preparation for sleep."
Nobody had noticed that before, said de Lecea. "This is the first finding of a sleep-preparation starter site in the brain. It's likely we humans have one, too. If we're disrupting this preparation by, say, reading email or playing videogames, which not only give off light but charge up our emotions and get our VTA dopaminergic circuitry going, it's easy to see why we're likely to have trouble falling asleep."
Noting that this anticipatory phase is often at the root of many people's sleeping problems, de Lecea suggested that the newly identified circuit could be a target for pharmacological intervention to help people ease into sleep.
"We have plenty of drugs that counter dopamine," he said. "Perhaps giving a person the right dose, at just the right time, of a drug with just the right pharmacokinetic properties so its effect will wear off at the right time would work a lot better than bombarding the brain with benzodiazepines, such as Valium, that knock out the entire brain."
He said he also sees the possibility that drugs targeting the VTA's dopamine-secreting nerve cells could benefit those suffering from neurological conditions such as schizophrenia or bipolar disorder that are characterized by sleep-wake cycle disturbances.
"It could be that merely solving the sleep-wake part will clear up a lot of symptoms," de Lecea said.
https://www.sciencedaily.com/releases/2016/09/160905114515.htm
A new angle on anxiety Surprising findings specific brain cells as the key target
September 6, 2016
Science Daily/Boston Children's Hospital
Clinical anxiety affects up to 30 percent of Americans who are in great need of better treatments with fewer side effects. A study finds that certain neurons in the hypothalamus play a central, previously unknown role in triggering anxiety.
https://images.sciencedaily.com/2016/09/160906084828_1_540x360.jpg
In the 'gangplank' experiment, for example, the genetically altered mice were perfectly willing to venture onto an elevated maze, even the 'open' section whose protective walls were removed
Credit: Boston Children's Hospital
Experiments in mice showed that blocking the stress hormone corticotropin-releasing hormone (CRH) selectively in this group of neurons erased the animals' natural fears. Mice with the deletion readily walked elevated gangplanks, explored brightly lit areas and approached novel objects -- things normal mice avoid.
CRH, discovered nearly 40 years ago, coordinates our physical and behavioral stress response, often termed the "fight-or-flight" response. This response helps us survive in the face of threats, but when it is activated at the wrong time or too intensely, it can lead to anxiety and/or depression.
For this reason, several drug companies have developed CRH-blocking drugs as possible alternatives to SSRIs and benzodiazepines, which have side effects, for treating anxiety disorders. However, the results have been disappointing: of the eight completed phase II and III trials of CRH antagonists for depression or anxiety, six have been published, with largely negative findings, says Majzoub.
Zhang had a hunch that blocking CRH throughout the brain, as was done in the above drug trials, isn't the best approach. "Blocking CRH receptors all over the brain doesn't work," she says. "We think the effects work against each other somehow. It may be that CRH has different effects depending on where in the brain it is produced."
Using genetic engineering, Zhang and her colleagues selectively removed the CRH gene from about 1,000 nerve cells in the hypothalamus of mice. (To do this, they used a genetic trick, knocking out the gene only in cells expressing another gene called SIM1.)
The targeted cells were in the paraventricular nucleus, an area of the hypothalamus known to control the release of stress hormones (such as cortisol). But to Zhang's surprise, the loss of CRH in those cells affected not only hormone secretion, but also dramatically reduced anxiety behaviors (vigilance, suspicion, fear) in the mice.
"We already knew that CRH controlled the hormonal response, but the big surprise was that the behavioral response was completely blunted," says Majzoub. "It was a very robust finding: Every parameter we looked at indicated that this animal was much less inhibited."
In the "gangplank" experiment, for example, the genetically altered mice were perfectly willing to venture onto an elevated maze, even the "open" section whose protective walls were removed.
Similarly, when the mice were presented with an open field, the modified mice explored much more of its center, rather than hang out at the periphery like the control mice.
Another surprise was that CRH secreted in the paraventricular nucleus goes to more places in the brain than originally thought -- including areas that control the behavioral stress response. "It was a total surprise to us that the locus of control is in a tiny part of the hypothalamus," says Majzoub.
Majzoub acknowledges that blocking CRH production in just a subset of neurons would be technically challenging in humans. But if this could be done, it could be helpful for treating severe anxiety disorders or post-traumatic stress disorder (PTSD).
"Blocking just certain neurons releasing CRH would be enough to alter behavior in a major way," he says. "We don't know how to do that, but at least we have a starting point."
https://www.sciencedaily.com/releases/2016/09/160906084828.htm
Light causes drosophila to take longer midday nap
September 16, 2016
Science Daily/Julius-Maximilians-Universität Würzburg, JMU
Fruit flies' activity peaks especially in the morning and late afternoon. The insects extend their midday siesta on long summer days. Researchers have now found out what triggers this behavior. A miniature pair of eyelets discovered in the late 80s plays a crucial role in this context.
https://images.sciencedaily.com/2016/09/160916093047_1_540x360.jpg
The large compound eyes left and right are clearly recognizable in the head of the fruit fly. The four-cell Hofbauer-Buchner eyelet (yellow; only one eyelet shown in the drawing) is located underneath the compound eye. From the eyelets, nerve fibers (also yellow) run directly to the clock network in the fly's brain.
Credit: Team Helfrich-Förster
In 1989, the Würzburg biologists Alois Hofbauer and Erich Buchner reported a surprising finding in the journal "Naturwissenschaften": They had identified a new pair of eyelets in drosophila unknown until then. The fruit fly was considered an important model organism for zoologists and geneticists even back then with scores of scientists showing an interest in the tiny insect. But they had all failed to detect the additional eyes -- no wonder given their microscopic size: Each eyelet consists of just four photoreceptor cells.
In spite of this, the Hofbauer-Buchner eyelets seem to play a major role in the life of drosophila. A study conducted by scientists from the University of Würzburg with colleagues from the University of Michigan and the University of Bristol has come to this conclusion.
Drosophila's activity peaks in the morning and in the late afternoon and they rest during the hottest time of the day. The tiny sensory organs evidently influence when this midday siesta ends. "On long summer days, they delay the onset of the afternoon activity phase," explains Professor Charlotte Helfrich-Förster from the University of Würzburg's Biocenter.
Hardwired in the fly's brain
The scientist has studied drosophila's circadian rhythms for years. In the current study, her research team has been able to show for the first time that the Hofbauer-Buchner eyelets are wired to a clock neuron network in the flies' brain: Nerve fibres run directly from the eyelets to two groups of clock neurons. One of them is responsible for the morning activity whereas the other influences the evening activity.
"At daybreak, light falls onto the eyelets," Helfrich-Forster details. "This light input triggers the production of the two neurotransmitters histamine and acetylcholine. We suppose that acetylcholine activates the neurons relevant for morning activity. At the same time, the histamine seems to indirectly inhibit the circadian clock for the evening peak phase thereby extending the phase of inactivity." Hence, the Hofbauer-Buchner eyelets are part of a complex network that governs drosophila's sleep/activity rhythm.
Mammalian clock similar to that of flies
Another reason why the findings are interesting is because the circadian clocks of animals have changed comparably little in the course of evolution. "Mice, for example, have a neuronal clock network in their brains that shares many similarities with that of the fruit fly," Helfrich-Förster emphasises. "Therefore, drosophila allows us to get deep insights into the circadian clock of mammals and probably into that of humans, too."
https://www.sciencedaily.com/releases/2016/09/160916093047.htm
Lack of interest in sex successfully treated by exposure to bright light
September 18, 2016
Science Daily/European College of Neuropsychopharmacology (ECNP)
Exposure to bright light increases testosterone levels and leads to greater sexual satisfaction in men with low sexual desire. These are the results of a pilot randomised placebo-controlled trial.
Low sexual desire affects significant numbers of men after the age of 40, with studies finding that up to 25% of men report problems*, depending on age and other factors. Scientists had previously noted that sexual interest varies according to the seasons, prompting the idea that levels of ambient light may contribute to sexual desire.
Now a group of scientists from the University of Siena in Italy have tested sexual and physiological responses to bright light. They found that regular, early-morning, use of a light box -- similar to those used to combat Seasonal Affective Disorder -- led both to increased testosterone levels and greater reported levels of sexual satisfaction.
The scientists, led by Professor Andrea Fagiolini, took recruited 38 men who had been attending the Urology Department of the University of Siena following a diagnosis of hypoactive sexual desire disorder or sexual arousal disorder -- both conditions which are characterised by a lack of interest in sex. Each man underwent an initial evaluation to determine the baseline level of interest in sex, with testosterone levels also being measured.
The researchers then divided the men into two groups. One group received regular treatment with a specially adapted light box, the control (placebo) group was treated via a light box which had been adapted to give out significantly less light. Both groups were treated early in the morning, with treatment lasting half an hour per day. After two weeks of treatment or placebo, the researchers retested sexual satisfaction and testosterone levels.
Professor Fagiolini said "We found fairly significant differences between those who received the active light treatment, and the controls. Before treatment, both groups averaged a sexual satisfaction score of around 2 out of 10, but after treatment the group exposed to the bright light was scoring sexual satisfaction scores of around 6.3 -- a more than 3-fold increase on the scale we used. In contrast, the control group only showed an average score of around 2.7 after treatment."
The researchers also found that testosterone levels increased in men who had been given active light treatment. The average testosterone levels in the control group showed no significant change over the course of the treatment -- it was around 2.3 ng/ml at both the beginning and the end of the experiment. However, the group given active treatment showed an increase from around 2.1 ng/ml to 3.6 ng/ml after two weeks.
Professor Fagiolini explained: "The increased levels of testosterone explain the greater reported sexual satisfaction. In the Northern hemisphere, the body's Testosterone production naturally declines from November through April, and then rises steadily through the spring and summer with a peak in October. You see the effect of this in reproductive rates, with the month of June showing the highest rate of conception. The use of the light box really mimics what nature does.
We believe that there may be several explanations to explain the underlying mechanism. For instance, light therapy inhibits the pineal gland in the centre of the brain and this may allow the production of more testosterone, and there are probably other hormonal effects. We're not yet at the stage where we can recommend this as a clinical treatment. Even at that stage, there will be a few patients -- for example those with an eye condition or anyone taking medicines which affect light sensitivity (some antidepressants, and some antibiotics, for example) -- who would need to take special care. However if this treatment can be shown to work in a larger study, then light therapy may offer a way forward. It's a small study, so for the moment we need to treat it with appropriate caution."
The researchers note that there are several possible reasons for lack of sexual desire. Treatment depends on the underlying cause, but current therapeutic options include testosterone injections, antidepressants, and other medications. The researchers believe that light therapy may offer the benefits of medication, but with fewer side effects.
Commenting, Professor Eduard Vieta (Chair of the Department of Psychiatry and Psychology at the University of Barcelona Hospital Clinic and treasurer of the ECNP) said: "Light therapy has been used successfully in the past to treat some forms of depression and this study suggests now that it may also work to treat low sexual desire in men. The mechanism of action appears to be related to the increase of testosterone levels. Before this kind of treatment, which is likely to be better tolerated than pharmacological therapy, gets ready for its routine use, there are many steps to be implemented, including replication of the results in a larger, independent study, and verifying whether the results are long-lasting and not just short-term."
https://www.sciencedaily.com/releases/2016/09/160918214443.htm