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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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Journal ArticleDOI
TL;DR: Since this polygraphic finding may be present in subjects without any sleep complaint and in patients with initial neurological impairment, diagnosis of the sleep disorders might be allowed only when the polygraphic characteristic of persistent tonus and complex motor behavior are recorded.

139 citations

Journal ArticleDOI
TL;DR: Clinical and basic neuroscience evidence indicates that RBD results from breakdown of the network underlying REM sleep atonia, and this finding is important because it opens new avenues for treating RBD and understanding its link to neurodegenerative disorders.

139 citations

Journal ArticleDOI
TL;DR: A role for the SCN is supported in the active promotion of REM sleep at specific times of day, such that transitions into REM sleep are facilitated by theSCN during the rest phase, but the amount of REMSleep, once initiated, is determined primarily by homeostatic mechanisms.
Abstract: The daily timing of rapid eye movement (REM) sleep reflects an interaction between the circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus (SCN) and a homeostatic process that induces compensatory REM sleep in response to REM sleep loss. Whether the circadian variation in REM sleep propensity is caused by active promotion, inhibition, or passive gating of REM sleep homeostasis by the SCN is unknown. To investigate these possibilities, compensatory responses to 24 hr REM sleep deprivation (RSD) were compared between SCN-lesioned (SCNx) and sham-lesioned rats at different times of day in constant dark. The attempts to enter REM sleep (REM tendency) increased during RSD in all rats and were modulated by circadian phase in sham-lesioned, but not SCNx rats. REM sleep homeostasis interacted with circadian time, such that REM tendency doubled during the rest phase in sham-lesioned rats relative to SCNx rats (F((6,93)) = 17.9; p = 0.0001). However, REM tendency was indistinguishable between SCNx and sham-lesioned rats during the activity phase, suggesting the SCN does not inhibit REM tendency at this time. By contrast, the amount of compensatory REM sleep examined 2, 6, 12, or 24 hr after RSD did not depend on circadian phase. Thus, transitions into REM sleep are facilitated by the SCN during the rest phase, but the amount of REM sleep, once initiated, is determined primarily by homeostatic mechanisms. This work supports a role for the SCN in the active promotion of REM sleep at specific times of day.

139 citations

Journal ArticleDOI
01 Jun 2009-Sleep
TL;DR: Learning to reach specifically affects gene expression in the trained motor cortex and, in the same area, increases sleep need as measured by a local change in SWA.
Abstract: Study objective: The best characterized marker of sleep homeostasis is the amount of slow wave activity (SWA, 05-4 Hz) during NREM sleep SWA increases as a function of previous waking time and declines during sleep, but the underlying mechanisms remain unclear We have suggested that SWA homeostasis is linked to synaptic potentiation associated with learning during wakefulness Indeed, studies in rodents and humans found that SWA increases after manipulations that presumably enhance synaptic strength, but the evidence remains indirect Here we trained rats in skilled reaching, a task known to elicit long-term potentiation in the trained motor cortex, and immediately after learning measured SWA and cortical protein levels of c-fos and Arc, 2 activity-dependent genes involved in motor learning Design: Intracortical local field potential recordings and training on reaching task Setting: Basic sleep research laboratory Patients or Participants: Long Evans adult male rats Interventions: N/A Measurements and Results: SWA increased post-training in the trained cortex (the frontal cortex contralateral to the limb used to learn the task), with smaller or no increase in other cortical areas This increase was reversible within 1 hour, specific to NREM sleep, and positively correlated with changes in performance during the prior training session, suggesting that it reflects plasticity and not just motor activity Fos and Arc levels were higher in the trained relative to untrained motor cortex immediately after training, but this asymmetry was no longer present after 1 hour of sleep Conclusion: Learning to reach specifically affects gene expression in the trained motor cortex and, in the same area, increases sleep need as measured by a local change in SWA

139 citations

Journal ArticleDOI
TL;DR: Nasal CPAP completely abolished all obstructive apneas and allowed apnea-free breathing in all 12 patients and significantly reduced stage I/II non-rapid eye movement (NREM) sleep and markedly increased stage III/IV NREM and REM sleep on the first treatment night.

138 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023229
2022453
2021353
2020283
2019315
2018221