Topic
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.
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TL;DR: In this paper, the authors developed a standardized protocol for delineating quasisteady-state pressure-flow relationships for the upper airway from which these variables could be derived, and investigated the effect of body position and sleep stage on these variables by determining Pcrit and RN, and their confidence intervals (CIs), for each condition.
120 citations
TL;DR: The hypothesis that REM-sleep timing is controlled by accumulation of REM- sleep propensity during NREM sleep is supported.
Abstract: Sleep structure in the rat was characterized during uninterrupted full-day recordings using an analytic procedure that identifies rapid eye movement (REM) sleep episodes based on REM-sleep-onset electroencephalograph phenomena, hence independently of REM-sleep duration. The data were used to determine whether REM-sleep timing is controlled homeostatically or by an oscillatory mechanism. The findings and conclusions are that 1) non-REM (NREM) sleep episode duration is positively correlated with prior REM-sleep episode duration, suggesting that REM-sleep expression is permissive of NREM sleep; 2) mean NREM-sleep episode duration decreases after repeated brief REM-sleep episodes ( 30 s), suggesting that REM-sleep propensity increases progressively within episodes of NREM sleep; and 5) the diurnal cycle of REM-sleep expression primarily reflects modulation in the efficiency of REM-sleep maintenance. These findings support the hypothesis that REM-sleep timing is controlled by accumulation of REM-sleep propensity during NREM sleep.
120 citations
TL;DR: The results show that in the rat a volley of electrical activity that is sufficiently strong to excite and recruit a large cortical neuronal population is capable of inducing slow waves during natural sleep.
Abstract: In humans, non-rapid eye movement (NREM) sleep slow waves occur not only spontaneously but can also be induced by transcranial magnetic stimulation. Here we investigated whether slow waves can also...
120 citations
TL;DR: Initial management should focus on decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders, and pharmacotherapy for other parasomnias is less certain, and further investigations are necessary.
119 citations
TL;DR: It is proposed that the change in sleep–wake regulation in the context of repeated sleep restriction reflects an allostatics process, and that the allostatic load produced by SD has direct effects on the sleep-wake regulatory system.
Abstract: Recent studies indicate that chronic sleep restriction can have negative consequences for brain function and peripheral physiology and can contribute to the allostatic load throughout the body. Interestingly, few studies have examined how the sleep–wake system itself responds to repeated sleep restriction. In this study, rats were subjected to a sleep-restriction protocol consisting of 20 h of sleep deprivation (SD) followed by a 4-h sleep opportunity each day for 5 consecutive days. In response to the first 20-h SD block on day 1, animals responded during the 4-h sleep opportunity with enhanced sleep intensity [i.e., nonrapid eye movement (NREM) delta power] and increased rapid eye movement sleep time compared with baseline. This sleep pattern is indicative of a homeostatic response to acute sleep loss. Remarkably, after the 20-h SD blocks on days 2–5, animals failed to exhibit a compensatory NREM delta power response during the 4-h sleep opportunities and failed to increase NREM and rapid eye movement sleep times, despite accumulating a sleep debt each consecutive day. After losing ≈35 h of sleep over 5 days of sleep restriction, animals regained virtually none of their lost sleep, even during a full 3-day recovery period. These data demonstrate that the compensatory/homeostatic sleep response to acute SD does not generalize to conditions of chronic partial sleep loss. We propose that the change in sleep–wake regulation in the context of repeated sleep restriction reflects an allostatic process, and that the allostatic load produced by SD has direct effects on the sleep–wake regulatory system.
119 citations