Non-rapid eye movement sleep

About: Non-rapid eye movement sleep is a research topic. Over the lifetime, 8661 publications have been published within this topic receiving 389465 citations. The topic is also known as: NREM.

Prostaglandin D2 in Sleep-Wake Regulation: Recent Progress and Perspectives:

Abstract: Prostaglandin (PG) D2 is one of the most active endogenous sleep-promoting substances, which induces physiological sleep in rodents, primates, and most probably in humans as well. In this update article, we review recent experimental results concerning the molecular mechanisms underlying sleep-wake regulation by PGD2, the link between the humoral regulation by the PGD2 system, and the neural network involved in the promotion of non-rapid eye movement (NREM) sleep and the abnormality of NREM sleep regulation found in gene-manipulated mice for PGD synthase.

Association Between Sleep Architecture and Measures of Body Composition

Abstract: THE PREVALENCE OF OBESITY IN THE US HAS DOUBLED OVER THE PAST 3 DECADES.1 DURING THIS SAME TIME PERIOD, SELF-REPORTED SLEEP DURATION has decreased,2,3 and it is estimated that only one-quarter of adults sleep ≥ 8 hours per day.3 A number of recent epidemiologic studies have suggested an association between total sleep time and the risk of obesity.4–7 Specifically, body mass index (BMI) has been shown to increase as total sleep duration decreases. However, few studies have assessed the relationship between sleep architecture and BMI. Sleep is regulated by 2 distinct processes: (1) a homeostatic process that depends on the amount of prior sleep and wakefulness; and (2) a circadian process that is driven by an endogenous pacemaker. Of the various stages of sleep, slow wave sleep (SWS) is the deepest stage and has the highest arousal threshold.8 In subjects with previous sleep loss, SWS appears to be preferentially recovered compared with REM sleep which may reflect increased homeostatic drive (i.e., sleep pressure).9 Studies have shown that on recovery nights following a period of sleep loss, there is first rebound and recuperation of SWS, after which recovery of other sleep stages occurs.10–13 Despite this preservation of SWS, its functional significance is unclear. It has been hypothesized that SWS is important for the consolidation of memory.14,15 The role of SWS in metabolism and energy conservation in human beings is unknown. Small clinical studies performed 20-30 years ago evaluated the relationship between REM sleep (but not SWS) and body weight, with inconsistent results.16–19 A recent small experimental study in healthy subjects showing insulin resistance occurring the morning after selective SWS sleep deprivation has provided intriguing data implicating SWS as a mediator of glucose homeostasis.20 We recently reported from the Outcomes of Sleep Disorders in Older Men study (MrOS Sleep Study) that decreased total sleep time (TST) assessed by actigraphy was related to increased odds of obesity.21 This study examines whether, in the same large cohort of community-dwelling older men, SWS specifically, rather than just TST, is associated with BMI and other measures of body composition, independent of confounding factors (including age, race, physical activity, sleep disordered breathing, and sleep efficiency). A secondary aim of this study was to determine whether REM sleep (as a percentage of TST) is associated with measures of body composition, independent of other confounding factors.

Abnormal sleep/wake dynamics in orexin knockout mice.

Abstract: OVER 20 YEARS AGO, BROUGHTON AND COLLEAGUES HYPOTHESIZED THAT NARCOLEPSY IS BEST CONSIDERED A DISEASE OF STATE BOUNDARY CONTROL.1 They argued that sleepiness, cataplexy, hallucinations, and many other symptoms could be viewed as a breakdown of “whatever neurochemical ‘glues' or integrative neurophysiological mechanisms exist for sleep and wake state continuity.”1 This hypothesis is compelling, but it has been difficult to examine using conventional sleep scoring methods. More recently, our understanding of narcolepsy has been greatly advanced by the discovery that narcolepsy with cataplexy is caused by a loss of functional signaling by the orexin (hypocretin) neuropeptides.2–5 The neurons producing orexins are active during wakefulness,6–8 and direct activation of these neurons can awaken mice from sleep.9 In addition, orexins probably stabilize wake and sleep; narcoleptic people, dogs, and mice lacking orexins have great difficulty remaining awake for long periods and also experience fragmented sleep.10–13 In earlier work, we found that the fragmented wakefulness of orexin deficiency is not a consequence of abnormal sleep homeostasis, poor circadian control, or defective fundamental arousal systems.10 However, conventional sleep scoring in 10- to 30-second epochs reveals little about the process of transitioning between states as cortical activity and behavior can change quite rapidly. Furthermore, conventional scoring simply identifies discrete states, so it can overlook important variations within states, such as the distinctions between light and deep NREM sleep or between drowsy wake and high levels of arousal. Therefore, to determine how orexin deficiency causes behavioral state instability we developed a state space analysis technique to examine the dynamics of sleep/wake behavior in orexin knockout (OXKO) mice, a model of narcolepsy. The previous application of state space techniques to sleep recordings used local field potential data, but the variability in these signals prevented comparisons between animals.14–16 We adapted these techniques for analysis of EEG recordings in mice and developed metrics for inter-animal comparisons. State space techniques have high temporal resolution and analyze behavior as a continuum, rather than in discrete states, thus facilitating higher dimensional examination of state transitions. This approach enabled us to determine whether the state instability in this mouse model of narcolepsy reflects abnormal sleep/wake states, faster movements between states, or abnormal transition processes.

Disturbed sleep while being on-call: an EEG study of ships' engineers.

Abstract: In order to investigate the effects of on-call duty on sleep and wakefulness, five male ships' engineers were studied using electroencephalogram (EEG) and electrocardiogram (ECG) recordings and subjective ratings. Sleep during on-call nights (two alarms) was shortened and contained less slow wave sleep (SWS) and rapid eye movement (REM) sleep, lower spectral power density, and a higher heart rate. Many of the effects were observable before any alarms had occurred. Rated sleep quality was lower, and sleepiness was higher during the subsequent day. It was suggested that the effects were due to apprehension/uneasiness induced by the prospect of being awakened by an alarm.