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The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of ß-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.

Visual imagery during sleep has long been a topic of persistent speculation, but its private nature has hampered objective analysis. Here we present a neural decoding approach in which machine-learning models predict the contents of visual imagery during the sleep-onset period, given measured brain activity, by discovering links between human functional magnetic resonance imaging patterns and verbal reports with the assistance of lexical and image databases. Decoding models trained on stimulus-induced brain activity in visual cortical areas showed accurate classification, detection, and identification of contents. Our findings demonstrate that specific visual experience during sleep is represented by brain activity patterns shared by stimulus perception, providing a means to uncover subjective contents of dreaming using objective neural measurement.

Key Points Sleep promotes the consolidation of declarative as well as procedural and emotional memories in a wide variety of tasks. Sleep improves preferentially the consolidation of memories that were encoded explicitly and are behaviourally relevant to the individual. Consolidation during sleep not only strengthens memory traces quantitatively but can also produce qualitative changes in memory representations. An active process of re-organization enables the formation of new associations and the extraction of generalized features. This can ease novel inferences and insights. Spatio-temporal patterns of neuronal activity during encoding in the awake state become re-activated during subsequent sleep, specifically during slow-wave sleep (SWS) which is a state of minimum cholinergic activity. Such re-activations might promote the gradual redistribution of hippocampus-dependent memories from the hippocampus to neocortical sites for long-term storage (system consolidation) and might also trigger enduring synaptic changes to stabilize memories (synaptic consolidation). Neocortical (<1 Hz) slow oscillations, thalamo-cortical spindles and hippocampal sharp-wave ripples are implicated in memory consolidation during SWS. The depolarizing up-states of the slow oscillations synchronously drive the generation of spindles and ripples accompanying hippocampal memory re-activations, thus providing a temporal frame for a fine-tuned hippocampus-to-neocortex transfer of memories. Neocortical slow oscillations concurrently support a global synaptic downscaling that precludes saturation of synaptic networks and improves the capacity to encode new information. Rapid eye movement (REM) sleep is characterized by a local upregulation of plasticity-related immediate early genes in the presence of high cholinergic activity and reduced electroencephalographic coherence between brain regions. These conditions might effectively support local synaptic consolidation. The temporal sequence of SWS and REM sleep in the normal sleep cycle suggests that these sleep stages have complementary roles in memory consolidation: during SWS, system consolidation promotes the re-activation and redistribution of select memory traces for long-term storage, whereas ensuing REM sleep might act to stabilize the transformed memories by enabling undisturbed synaptic consolidation. Sleep improves the consolidation of both declarative and non-declarative memories. Diekelmann and Born discuss the potential mechanisms through which slow wave sleep and rapid eye movement sleep support system and synaptic consolidation. Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory, depending on the specific conditions of learning and the timing of sleep. Consolidation during sleep promotes both quantitative and qualitative changes of memory representations. Through specific patterns of neuromodulatory activity and electric field potential oscillations, slow-wave sleep (SWS) and rapid eye movement (REM) sleep support system consolidation and synaptic consolidation, respectively. During SWS, slow oscillations, spindles and ripples — at minimum cholinergic activity — coordinate the re-activation and redistribution of hippocampus-dependent memories to neocortical sites, whereas during REM sleep, local increases in plasticity-related immediate-early gene activity — at high cholinergic and theta activity — might favour the subsequent synaptic consolidation of memories in the cortex.

The interrelationship between circadian and sleep rhythm abnormalities and neurological disease has long been recognized. Foster and colleagues now provide a conceptual framework regarding common mechanisms of neurological disease and circadian and sleep physiology, and propose new approaches for the treatment of neuropsychiatric and neurodegenerative diseases. Sleep and circadian rhythm disruption are frequently observed in patients with psychiatric disorders and neurodegenerative disease. The abnormal sleep that is experienced by these patients is largely assumed to be the product of medication or some other influence that is not well defined. However, normal brain function and the generation of sleep are linked by common neurotransmitter systems and regulatory pathways. Disruption of sleep alters sleep–wake timing, destabilizes physiology and promotes a range of pathologies (from cognitive to metabolic defects) that are rarely considered to be associated with abnormal sleep. We propose that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms. The stabilization of sleep may be a means by which to reduce the symptoms of — and permit early intervention of — psychiatric and neurodegenerative disease.

Insufficient sleep and poor quality sleep are pervasive during adolescence and relate to impairments in cognitive control and increased risk taking. However, the neurobiology underlying the association between sleep and adolescent behavior remains elusive. In the current study, we examine how poor sleep quality relates to cognitive control and reward related brain function during risk taking. Forty-six adolescents participated in a functional magnetic imaging (fMRI) scan during which they completed a cognitive control and risk taking task. Behaviorally, adolescents who reported poorer sleep also exhibited greater risk-taking. This association was paralleled by less recruitment of the dorsolateral prefrontal cortex (DLPFC) during cognitive control, greater insula activation during reward processing, and reduced functional coupling between the DLPFC and affective regions including the insula and ventral striatum during reward processing. Collectively, these results suggest that poor sleep may exaggerate the normative imbalance between affective and cognitive control systems, leading to greater risk-taking in adolescents. ► Poor quality sleep is associated with adolescent risk taking behavior. ► Poor sleep disrupts brain function related to cognitive control and reward processing. ► Poor sleep may amplify the neural imbalance between affect and cognitive control.

Mice subjected to an aberrant daily light cycle that still maintain the circadian timing system are shown to exhibit increased depression-like behaviours and disruptions in synaptic plasticity and cognitive function. Disrupted light–dark cycles cause depression Disruption of the body's circadian clock by exposure to irregular light cycles can affect sleep–wake patterns and cause sleep deprivation, both of which are often associated with mood alterations and cognitive disruptions. This study in mice shows that irregular light schedules can directly affect mood and cognitive function, independent of sleep and circadian rhythms. The aberrant light effects are dependent on melanopsin-containing retinal ganglion cells, and administration of antidepressant drugs restores learning ability, suggesting that the depressive effect precedes learning impairment. The daily solar cycle allows organisms to synchronize their circadian rhythms and sleep–wake cycles to the correct temporal niche 1 . Changes in day-length, shift-work, and transmeridian travel lead to mood alterations and cognitive function deficits 2 . Sleep deprivation and circadian disruption underlie mood and cognitive disorders associated with irregular light schedules 2 . Whether irregular light schedules directly affect mood and cognitive functions in the context of normal sleep and circadian rhythms remains unclear. Here we show, using an aberrant light cycle that neither changes the amount and architecture of sleep nor causes changes in the circadian timing system, that light directly regulates mood-related behaviours and cognitive functions in mice. Animals exposed to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of corticosterone are increased. Despite normal circadian and sleep structures, these animals show increased depression-like behaviours and impaired hippocampal long-term potentiation and learning. Administration of the antidepressant drugs fluoxetine or desipramine restores learning in mice exposed to the aberrant light cycle, suggesting that the mood deficit precedes the learning impairments. To determine the retinal circuits underlying this impairment of mood and learning, we examined the behavioural consequences of this light cycle in animals that lack intrinsically photosensitive retinal ganglion cells. In these animals, the aberrant light cycle does not impair mood and learning, despite the presence of the conventional retinal ganglion cells and the ability of these animals to detect light for image formation. These findings demonstrate the ability of light to influence cognitive and mood functions directly through intrinsically photosensitive retinal ganglion cells.

The integration of segregated brain functional modules is a prerequisite for conscious awareness during wakeful rest. Here, we test the hypothesis that temporal integration, measured as long-term memory in the history of neural activity, is another important quality underlying conscious awareness. For this aim, we study the temporal memory of blood oxygen level-dependent signals across the human nonrapid eye movement sleep cycle. Results reveal that this property gradually decreases from wakefulness to deep nonrapid eye movement sleep and that such decreases affect areas identified with default mode and attention networks. Although blood oxygen level-dependent spontaneous fluctuations exhibit nontrivial spatial organization, even during deep sleep, they also display a decreased temporal complexity in specific brain regions. Conversely, this result suggests that long-range temporal dependence might be an attribute of the spontaneous conscious mentation performed during wakeful rest.

Purpose The Pittsburgh Sleep Quality Index (PSQI) is a self-reported questionnaire that measures sleep quality during the previous month. The aims of this study were to analyze the reliability and validity of the Korean version of the PSQI (PSQI-K) and to evaluate its usefulness. Methods We developed the PSQI-K, which involved translating the original PSQI into Korean and then translating back into English to check its accuracy. We tested the validity of the PSQI-K on a total of 394 individuals: 261 with poor sleep (primary insomnia, n  = 211; narcolepsy, n  = 50) and 133 with good sleep. All subjects completed the PSQI-K, 285 had overnight nocturnal polysomnography, and 53 were randomly selected for a retest with the questionnaire after 2–4 weeks without any intervening treatment. The mean PSQI-K global scores in each group were analyzed after adjusting for age and sex. Results Cronbach's α coefficient for internal consistency of the total score of the PSQI-K was 0.84 which shows high reliability. Sensitivity and specificity for distinguishing poor and good sleepers were 0.943 and 0.844 using the best cutoff point of 8.5. The total and component scores of the PSQI-K for insomnia and narcolepsy were significantly higher than those for controls ( p  < 0.05). The test–retest correlation coefficient was 0.65 for the total score ( p  < 0.001). There was no significant difference between the two values using the paired t tests. Conclusions The PSQI-K is a reliable and valid questionnaire for evaluating sleep quality in patients with sleep disorders.

Sleepers awake A paper published in Nature in April raised the intriguing possibility that optical therapies might be developed to treat neurological disorders. That work, in tissue slices and in C. elegans roundworms, showed that brain cells can be genetically engineered to alter their activity in response to pulses of different colours of light. A follow-up study now shows that behaviour can be modified in a living mammal by similar means. Hypocretin (Hcrt)-producing neurons in the hypothalamus are active during transitions from sleep to waking states. Optical stimulation of mouse Hcrt neurons engineered to respond to light increases the likelihood of transition from sleep to wakefulness, with higher frequencies causing more abrupt awakening. As Hcrt deficiency is linked to narcolepsy, these results may provide insights into sleep disorders. The neural underpinnings of sleep involve interactions between sleep-promoting areas such as the anterior hypothalamus, and arousal systems located in the posterior hypothalamus, the basal forebrain and the brainstem 1 , 2 . Hypocretin 3 (Hcrt, also known as orexin 4 )-producing neurons in the lateral hypothalamus 5 are important for arousal stability 2 , and loss of Hcrt function has been linked to narcolepsy 6 , 7 , 8 , 9 . However, it is unknown whether electrical activity arising from Hcrt neurons is sufficient to drive awakening from sleep states or is simply correlated with it. Here we directly probed the impact of Hcrt neuron activity on sleep state transitions with in vivo neural photostimulation 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , genetically targeting channelrhodopsin-2 to Hcrt cells and using an optical fibre to deliver light deep in the brain, directly into the lateral hypothalamus, of freely moving mice. We found that direct, selective, optogenetic photostimulation of Hcrt neurons increased the probability of transition to wakefulness from either slow wave sleep or rapid eye movement sleep. Notably, photostimulation using 5–30 Hz light pulse trains reduced latency to wakefulness, whereas 1 Hz trains did not. This study establishes a causal relationship between frequency-dependent activity of a genetically defined neural cell type and a specific mammalian behaviour central to clinical conditions and neurobehavioural physiology.

Short sleep duration is associated with impaired glucose tolerance and an increased risk of diabetes. The effects of sleep restriction on insulin sensitivity have not been established. This study tests the hypothesis that decreasing nighttime sleep duration reduces insulin sensitivity and assesses the effects of a drug, modafinil, that increases alertness during wakefulness. This 12-day inpatient General Clinical Research Center study included 20 healthy men (age 20-35 years and BMI 20-30 kg/m(2)). Subjects spent 10 h/night in bed for >or=8 nights including three inpatient nights (sleep-replete condition), followed by 5 h/night in bed for 7 nights (sleep-restricted condition). Subjects received 300 mg/day modafinil or placebo during sleep restriction. Diet and activity were controlled. On the last 2 days of each condition, we assessed glucose metabolism by intravenous glucose tolerance test (IVGTT) and euglycemic-hyperinsulinemic clamp. Salivary cortisol, 24-h urinary catecholamines, and neurobehavioral performance were measured. IVGTT-derived insulin sensitivity was reduced by (means +/- SD) 20 +/- 24% after sleep restriction (P = 0.001), without significant alterations in the insulin secretory response. Similarly, insulin sensitivity assessed by clamp was reduced by 11 +/- 5.5% (P < 0.04) after sleep restriction. Glucose tolerance and the disposition index were reduced by sleep restriction. These outcomes were not affected by modafinil treatment. Changes in insulin sensitivity did not correlate with changes in salivary cortisol (increase of 51 +/- 8% with sleep restriction, P < 0.02), urinary catecholamines, or slow wave sleep. Sleep restriction (5 h/night) for 1 week significantly reduces insulin sensitivity, raising concerns about effects of chronic insufficient sleep on disease processes associated with insulin resistance.