What is the mechanism behind unihemispheric sleep in animals?

What is the mechanism behind unihemispheric sleep in animals?

It is known that dolphins have the ability to sleep with only one half of their brain at a time.

According to this popular science source:

Dolphins sleep by resting one half of their brain at a time. This is called unihemispheric sleep. The brain waves of captive dolphins that are sleeping show that one side of the dolphin's brain "awake" while the other in a deep sleep ("slow-wave sleep"). Also, during this time, one eye is open (the eye opposite the sleeping half of the brain) while the other is closed.

Given that the dolphin probably depends on bilateral brainstem mechanisms for respiration, my assumption is that this "shutting down" mainly involves the cortex.

  • Is this true, or are areas like the thalamus also suppressed unilaterally?
  • How is this "switching" (from hemisphere to hemisphere) managed? Is it accomplished at the level of the thalamus, or within the brainstem?
  • Were a dolphin to be dominant in one hemisphere (surely Flipper was "right-finned"?), how is the representation of the dominant side of the body managed when the opposite cortex is suppressed?

In general, I don't think the answers to these questions are known. This paper is a good review of unihemispheric slow-wave sleep (USWS); the section on neurophysiological mechanisms is largely speculation based on how slow-wave sleep is generally thought to function--despite its lack of answers, that section is good reading anyhow, since it covers current evidence (in 2000, anyway!) and lines of inquiry. I dug through its citing articles as well, hoping for a more informative update; the best I found was this paper, which shows small differences (which may or may not be statistically significant) between the openness of the ipsi & contralateral eyes to the sleeping hemisphere based on right/left--which does suggest at least some hemispheric dominance at play. Eared seals also sleep on their side during USWS, and leave the sleeping side of the body out of the water, while the awake side of the body paddles to keep their nostrils from submerging; I found nothing suggesting hemispheric dominance issues there, though.

As far as hemisphere-switching mechanisms go, that first paper mentions work finding that unihemispheric slow-wave sleep develops only following sagittal transsection of the lower brainstem in cats--even when the interhemispheric commissures were not involved; that implies some kind of uncoupling of lower brainstem sleep regions, but that's about as far as anybody's got (or as far as I could find!).

An interesting question! If you find more work, come back and tell me about it.

1 Rattenborg, Amlaner, & Lima (2000). Behavioral, neurophysiological and evolutionary perspectives on unihemispheric sleep. Neuroscience & Biobehavioral Reviews Volume 24, Issue 8, December 2000, Pages 817-842.
2 Lyamin, O., & al. (2002). Unihemispheric slow wave sleep and the state of the eyes in a white whale. Behavioural Brain Research Volume 129, Issue 1-2, 1 February 2002, Pages 125-129.

Key mechanism behind sleep discovered: Finding holds promise for treatment of fatigue and sleep disorders

Washington State University researchers have discovered the mechanism by which the brain switches from a wakeful to a sleeping state. The finding clears the way for a suite of discoveries, from sleeping aids to treatments for stroke and other brain injuries.

"We know that brain activity is linked to sleep, but we've never known how," said James Krueger, WSU neuroscientist and lead author of a paper in the latest Journal of Applied Physiology. "This gives us a mechanism to link brain activity to sleep. This has not been done before."

The mechanism -- a cascade of chemical transmitters and proteins -- opens the door to a more detailed understanding of the sleep process and possible targets for drugs and therapies aimed at the costly, debilitating and dangerous problems of fatigue and sleeplessness. Sleep disorders affect between 50 and 70 million Americans, according to the Institute of Medicine of the National Academies. The Institute also estimates the lost productivity and mishaps of fatigue cost businesses roughly $150 billion, while motor vehicle accidents involving tired drivers cost at least $48 billion a year.

The finding is one of the most significant in Krueger's 36-year career, which has focused on some of the most fundamental questions about sleep.

Even before the dawn of science, people have known that wakeful activity, from working to thinking to worrying, affects the sleep that follows. Research has also shown that, when an animal is active and awake, regulatory substances build up in the brain that induce sleep.

"But no one ever asked before: What is it in wakefulness that is driving these sleep regulatory substances?" said Krueger. "No one ever asked what it is that's initiating these sleep mechanisms. People have simply not asked the question."

The researchers documented how ATP (adenosine triphosphate), the fundamental energy currency of cells, is released by active brain cells to start the molecular events leading to sleep. The ATP then binds to a receptor responsible for cell processing and the release of cytokines, small signaling proteins involved in sleep regulation.

By charting the link between ATP and the sleep regulatory substances, the researchers have found the way in which the brain keeps track of activity and ultimately switches from a wakeful to sleeping state. For example, learning and memory depend on changing the connections between brain cells. The study shows that ATP is the signal behind those changes.

The finding reinforces a view developed by Krueger and his colleagues that sleep is a "local phenomenon, that bits and pieces of the brain sleep" depending on how they've been used.

The link between sleep, brain cell activity and ATP has many practical consequences, Krueger said.

  • The study provides a new set of targets for potential medications. Drugs designed to interact with the receptors ATP binds to may prove useful as sleeping pills.
  • Sleep disorders like insomnia can be viewed as being caused by some parts of the brain being awake while other parts are asleep, giving rise to new therapies.
  • ATP-related blood flow observed in brain-imaging studies can be linked to activity and sleep.
  • Researchers can develop strategies by which specific brain cell circuits are oriented to specific tasks, slowing fatigue by allowing the used parts of the brain to sleep while one goes about other business. It may also clear the way for stroke victims to put undamaged regions of their brains to better use.
  • Brain cells cultured outside the body can be used to study brain cell network oscillations between sleep-like and wake-like states, speeding the progress of brain studies.

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Materials provided by Washington State University. Note: Content may be edited for style and length.

Neural mechanisms of the reinforcing action of cocaine

Cocaine has multiple central and peripheral pharmacological actions. The action responsible for the rewarding property, and hence the abuse liability, of cocaine is an action in the dopaminergic synapse in the rat the major set of critical dopaminergic synapses appears to be in the nucleus accumbens. Cocaine prolongs the activity of dopamine in the synapse by blocking the dopamine reuptake mechanism (which usually inactivates the transmitter by removing it from the proximity of its synaptic targets). This is an action shared with amphetamine in addition to blocking the dopamine reuptake mechanism, amphetamine also augments dopaminergic function by augmenting dopamine release directly into the synapse. While amphetamine and cocaine have discriminable subjective effects, perhaps due to differences in rate of onset and metabolism or perhaps due to different side effects, cocaine shares its rewarding impact and abuse liability very closely with amphetamine. When drug access is unlimited, cocaine and amphetamine have the same ability to dominate behavior, reducing other behaviors such as feeding and sleeping and, in the process, reducing stress resistance to life-threatening levels. Opiates also owe their reinforcing properties to their ability to activate dopaminergic synapses in brain reward circuitry, though they activate the system at a different site and by a different local mechanism than those of amphetamine and cocaine. Where amphetamine and cocaine activate dopaminergic activity in the dopaminergic synapse, opiates activate dopaminergic activity by activating (or disinhibiting) the dopaminergic cell bodies. The site of rewarding action of opiates is the ventral tegmental area, where the dopaminergic cells projecting to the nucleus accumbens (as well as other targets) are located. Opiate actions that are restricted to this mechanism do not include opiate physical dependence the dependence syndrome involves anatomically distinct systems in the brain, systems not activated by amphetamine or cocaine. While opiate physical dependence may contribute to the motivation for opiate intake in dependent subjects, it is not necessary for opiates to be habit-forming. The neural circuitry involved in the rewarding actions of cocaine, amphetamine, and the opiates is circuitry thought to be specialized for natural reward function. The circuit activated by these drugs is also activated by some cases of rewarding brain stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanisms behind 'Mexican waves' in the brain are revealed by scientists

Credit: Rice University

Scientists have revealed the mechanisms that enable certain brain cells to persuade others to create 'Mexican waves' linked with cognitive function.

Ultimately, the team say their work may help researchers understand more about normal brain function and about neurocognitive disorders such as dementia.

Neurons are cells in the brain that communicate chemical and electrical information and they belong to one of two groups- inhibitory or excitatory. While much is known about excitatory neurons, the role of inhibitory neurons is still being debated.

Inhibitory neurons can vibrate and they are equipped with mechanisms that enable them to persuade networks of other neurons into imitating their vibrations - setting off 'Mexican waves' in the brain. The scientists believe these collective, oscillating vibrations play a key role in cognitive function. Their research sheds light on how inhibitory neurons use different communication processes to excitatory neurons, which share information via an internal pulsing mechanism.

This study was carried out by Imperial College London and the Max Planck Institute for Brain Research. It is published today in the journal Nature Communications.

Dr Claudia Clopath, co-author from the Department of Bioengineering at Imperial College London, said: "These brain cells are similar to spectators in a football stadium, encouraging others into imitating them in a Mexican wave. We suspect that there is a very close relationship between the collective vibrations that they set off and many important cognitive functions. When the vibrations are degraded so that the wave is disrupted, we think it may contribute to neurocognitive disorders such as dementia. Our hope is that ultimately our research will lead to new insights into these disorders and how they can be treated."

The researchers developed a mathematical model showing the two mechanisms that inhibitory neurons need in order to convince others to join them in their rhythmical vibrations. The first is the mechanism that enables the inhibitory neurons to vibrate on their own, known as sub threshold resonance.

The second mechanism is a nanoscopic hole known as a gap-junction. There are many of these on the surface of the inhibitory neuron and they allow neurons to communicate directly with one another, enabling inhibitory neurons to set off a collective vibration.

The fact that inhibitory neurons are able to determine how and when whole networks of neurons will vibrate suggests that they are much more important in brain function than scientists had previously thought, say the researchers.

Now that the team have described the mechanisms behind these vibrations, the next step will see them carrying out research on inhibitory neurons to fully understand why vibrations are important for cognitive functions. The team believe that there may ultimately be a way to manipulate inhibitory neurons to improve how they vibrate, which might one day lead to better treatments for people with neurocognitive diseases.

What is the mechanism behind unihemispheric sleep in animals? - Psychology

Consciousness or awareness of the external environment is the line drawn between wakefulness and sleep. Falling asleep and losing consciousness involves a gradual progress of stages. A fully alert and awake individual is in stage 0. Stage 1 is accompanied by being drowsy and drifting in and out of sleep. Then the individual enters stages 2, followed by 3, and eventually 4. After stage 4 he/she will reverse the sequence by returning to stage 3, followed by 2, then 1-REM (rapid eye movement). This cycle takes between 90 to 120 minutes, due to individual differences, then repeats itself. Therefore, in 7 to 8 hours of sleep, this cycle repeats about 5 times (Franken, 1994).

To explain these stages in more detail, brain wave patterns recorded by EEG machines are useful. During wakefulness or at stage 0, alpha and beta activities are experienced in the human brain. Alpha activities consist of medium frequency waves. Beta activities consist of irregular low amplitude waves which are present when the individual is very alert and attentive. As the individual gets drowsy and enters stage 1, brain experiences theta activities. This is the transition stage between wakefulness and sleep. Stage 2 sleep contains irregular theta activities where sleep spindles (short bursts of waves of 12-14 Hz) and K complexes (sudden sharp wave forms) are present. Stage 3 sleep contains high-amplitude delta activities 20 to 50 percent of the time. Stage 4 is very similar to stage 3. It also contains delta activities however, they are present for more than 50 percent of the time. About 90 minutes after the onset of sleep, when the individual enters REM sleep, EEG patterns become very similar to those obtained during stage 1 sleep.

During REM sleep brain waves indicate theta activities which are very desynchronized (desynchronized means unregulated, e.g. trying to listen to several conversations simultaneously). This stage is also referred to as paradoxical sleep since brain activities during REM are comparable to those during wakefulness. REM lasts about 20 to 30 minutes. In 7 to 8 hours of sleep about 2 REMs are experienced (Carlson, 1991).

Although the entire nervous system becomes very active during REM, movements such as walking and talking are not present, because the muscles become atonic or paralyzed (Franken, 1994). This is due to the function of "locomotor centre" which produces paralysis in voluntary muscles. If this region is destroyed, the animal will move around during REM sleep (Horne, 1988).

In addition to changes in brain wave patterns, brain chemicals also fluctuate during sleep. The two major neurotransmitters involved in sleep are serotonin and norepinephrine. At the onset of sleep serotonin is secreted which increases NREM (non-rapid eye movement, stage 1 - 4 sleep). Secretion of norepinephrine takes place during REM resulting in increase of REM. Fluctuation between stages of sleep are thought to be due to secretion of these two neurotransmitters (Franken, 1994). Notably, a successful treatment of depression is to awaken the patient at the onset of REM sleep. This regulates the imbalance of norepinephrine and serotonin, alleviating depression (Carlson, 1991). However, additional findings about REM deprivation suggest an increase in aggression which lasts after REM deprivation is discontinued (Ellman & Antrobus, 1991).

At this point, it is important to discuss some of the experiments performed on humans and other animals involving sleep deprivation. In a study with human subjects Dinges and Kribbs discovered that performance on short tasks is not impaired when individuals are sleep deprived however, performance on longer tasks which require sustained attention becomes impaired. In other experiments subjects report perceptual distortions or even hallucinations (Franken, 1994). Rechtschaffen's study on rats that were sleep deprived between 5 to 33 days showed severe effects. During the study, the rats began to look sick and stopped grooming themselves. They became weak and uncoordinated. Some of them died and some had to be sacrificed. On autopsy, enlarged adrenal glands, stomach ulcers, and fluid in lungs were found among these rats note that these are some of the signs of stress (Carlson, 1991).

  1. Circadian rhythm - This is naturally a 25 hour cycle which determines when humans fall asleep. However, this cycle has become synchronized to 24 hours to correspond with the daily activities and the environment surrounding people. The existence of this cycle is thought to be due to: a.) fluctuation in adrenaline such that increase in adrenaline is accompanied by wakefulness and decrease in adrenaline is followed by sleep, and b.) fluctuation in body temperature such that decrease in body temperature occurs during sleep, but as morning approaches body temperature increases. Therefore, since body temperature is low during sleep, energy is conserved. This could also explain why some animals hibernate.
  2. Environmental arousal - certain factors cause a state of arousal. When humans are in this state, sleep tends to be disrupted (e.g. stress).
  3. Sleep deprivation - when one is sleep deprived, he/she tends to fall asleep sooner the next time and remain asleep longer. It must be emphasized that individual differences play an important role in sleep cycles (Franken, 1994).
  • Sleep is an adaptive behavior. By sleeping, animals conserve energy and rest when food is not as available. This is another explanation for why certain animals hibernate when food is scarce. Moreover, it is used as a survival mechanism because predators are more difficult to be detected.
  • Sleep is a period of restoration. During sleep, after the first occurrence of delta activity, certain growth hormones are secreted which are not only crucial in animals' growth in infancy, but also they are essential in bodily tissue repairs. Furthermore, the body is given an opportunity to repair the wear and tear caused by activities during waking (Moorcroft, 1993).
  • Sleep allows for cognitive processes. Studies by McGaugh, Jensen, and Martinez suggests that poor retention of information occurs if individuals are sleep deprived prior to learning (Moorcroft, 1993). In addition, during sleep information is organized, consolidated, incorporated and stored.

Many theories have also been developed which attempt to explain the function of dreams. However, as much as all of these theories may be true, none fully determines the function of dreams. Could it be that we are trying to resolved the unresolved issues of our lives in dreams? Or perhaps, we are trying to reach an emotional balance since dreams are our means of communication between the unconscious and conscious (Moorcroft, 1993). The answer to the true function of dreams is still ambiguous.

From all the theories developed which attempt to explain why we sleep and wake-up, a conclusion may be drawn that sleep is not the motivation for cognitive processes, behavioral adaptation, and restoration to take place. But survival is the motive behind sleep. Sleeping is only the behavior which satisfies the motivation to continue and survive. Perhaps, this is how Charles Darwin would have approached it.

Unihemispheric sleep and asymmetrical sleep: behavioral, neurophysiological, and functional perspectives

Sleep is a behavior characterized by a typical body posture, both eyes' closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent process (local sleep).

Keywords: asymmetry birds dolphins seals sleep unihemispheric.


EEG recorded from occipital–parietal derivations.…

EEG recorded from occipital–parietal derivations. Notes: ( A ) EEG in a bottlenose…

Electrographic recordings of the Cape…

Electrographic recordings of the Cape fur seal. Notes: ( A ) Wakefulness (…

Posture that northern fur seal…

Posture that northern fur seal assumes during USWS in water. Notes: Seal lying…

Electrographic recordings in the domestic…

Electrographic recordings in the domestic chick during sleep. Notes: ( A ) Wakefulness…

Model of unihemispheric sleep. Notes:…

Model of unihemispheric sleep. Notes: In the shaded and clear areas are shown…

Brain mechanisms behind a debilitating sleep disorder

Normally muscles contract in order to support the body, but in a rare condition known as cataplexy the body's muscles "fall asleep" and become involuntarily paralyzed. Cataplexy is incapacitating because it leaves the affected individual awake, but either fully or partially paralyzed. It is one of the bizarre symptoms of the sleep disorder called narcolepsy.

"Cataplexy is characterized by muscle paralysis during cognitive awareness, but we didn't understand how this happened until now, said John Peever of the University of Toronto's Department of Cell & Systems Biology. "We have shown that the neuro-degeneration of the brain cells that synthesize the chemical hypocretin causes the noradrenaline system to malfunction. When the norandrenaline system stops working properly, it fails to keep the motor and cognitive systems coupled. This results in cataplexy -- the muscles fall asleep but the brain stays awake."

Peever and Christian Burgess, also of Cell & Systems Biology used hypocretin-knockout mice (mice that experience cataplexy), to demonstate that a dysfunctional relationship between the noradrenaline system and the hypocretin-producing system is behind cataplexy. The research was recently published in the journal Current Biology in September.

The scientists first established that mice experienced sudden loss of muscle tone during cataplectic episodes. They then administered drugs to systematically inhibit or activate a particular subset of adrenergic receptors, the targets of noradrenaline. They were able to reduce the incidence of cataplexy by 90 per cent by activating noradrenaline receptors. In contrast, they found that inhibiting the same receptors increased the incidence of cataplexy by 92 per cent. Their next step was to successfully link how these changes affect the brain cells that directly control muscles.

They found that noradrenaline is responsible for keeping the brain cells (motoneurons) and muscles active. But during cataplexy when muscle tone falls, noradrenaline levels disappear. This forces the muscle to relax and causes paralysis during cataplexy. Peever and Burgess found that restoring noradrenaline pre-empted cataplexy, confirming that the noradrenaline system plays a key role.

Chronic sleep deprivation and seasonality: implications for the obesity epidemic

Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation.


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Unraveling the Evolutionary Determinants of Sleep

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Does subjective sleep affect cognitive function in healthy elderly subjects? The Proof cohort

Some epidemiological data are available on the association between sleep duration and sleep quality, sleep complaints, and the aging related cognitive impairment in the elderly. In this study we examined a large sample of healthy elderly subjects to assess the relationship between sleep quality, subjective cognitive complaints, and neuropsychological performance.

A total of 272 elderly subjects (mean age 74.8 ± 1.1 years) were recruited from a population-based cross-sectional study on aging and cardiovascular morbidity. All subjects filled in self-assessment questionnaires evaluating cognitive function, anxiety, depression, sleep-related parameters, and the Pittsburgh Sleep Quality Index (PSQI). Ambulatory polygraphy and extensive neuropsychological tests were also performed. Based on the total PSQI score, subjects were classified as good sleepers (GS, PSQI < 5, n = 116) and poor sleepers (PS, PSQI ⩾ 5, n = 156).

Poor sleep did not affect the subjective cognitive function score, subjective cognitive impairment being mainly related to anxiety, depression, and sleep medication intake. No significant differences were seen between GS and PS in any of the objective cognitive function tests except for the Trail Making Test A (TMA-A), processing speed being longer in the PS group (p < 0.001). Neither the presence of sleep-related breathing disorders nor gender affected cognitive performance.

Our results suggest that in healthy elderly subjects, subjective sleep quality and duration did not significantly affect subjective and objective cognitive performances, except the attention level, for that the interference of sleep medication should be considered.

Whole brain white matter changes revealed by multiple diffusion metrics in multiple sclerosis: A TBSS study

To investigate whole brain white matter changes in multiple sclerosis (MS) by multiple diffusion indices, we examined patients with diffusion tensor imaging and utilized tract-based spatial statistics (TBSS) method to analyze the data.

Forty-one relapsing-remitting multiple sclerosis (RRMS) patients and 41 age- and gender-matched normal controls were included in this study. Diffusion weighted images were acquired by employing a single-shot echo planar imaging sequence on a 1.5 T MR scanner. Voxel-wise analyses of multiple diffusion metrics, including fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD) were performed with TBSS.

The MS patients had significantly decreased FA (9.11%), increased MD (8.26%), AD (3.48%) and RD (13.17%) in their white matter skeletons compared with the controls. Through TBSS analyses, we found abnormal diffusion changes in widespread white matter regions in MS patients. Specifically, decreased FA, increased MD and increased RD were involved in whole-brain white matter, while several regions exhibited increased AD. Furthermore, white matter regions with significant correlations between the diffusion metrics and the clinical variables (the EDSS scores, disease durations and white matter lesion loads) in MS patients were identified.

Widespread white matter abnormalities were observed in MS patients revealed by multiple diffusion metrics. The diffusion changes and correlations with clinical variables were mainly attributed to increased RD, implying the predominant role of RD in reflecting the subtle pathological changes in MS.

The experiment in this article was not formally preregistered. The MOSS is provided in the supplemental information. MOSS, statistics, data, and code are available at

This research was supported by grants from the Swedish Research Council for Humanities and Social Sciences, the Swedish Research Council for Health, Working Life and Welfare, and the Swedish Research Council.

Conflict of interest statement. Financial disclosures: K.P.W. reports funding from NIH, Office of Naval Research, Philips Inc., Torvec Inc Consulting fees from or served as a paid member of scientific advisory boards for NIH, CurAegis Inc. Circadian Therapeutics, Kellogg Speaker honorarium or travel reimbursement fees from the American Academy of Sleep Medicine, American College of CHEST Physicians, American College of Sports Medicine, Associated Professional Sleep Societies, Daylight Academy, Illuminating Engineering Society, and the Sleep Research Society. J.A. has current funding from the Swedish Research Council for Humanities and Social Sciences and AFA Insurance. Non-financial disclosure: None declared.