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Rapid eye movement sleep

About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.


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Journal ArticleDOI
01 Apr 2009-Chest
TL;DR: When RUA and blood gas disturbances are minimized by CPAP, genioglossal activity is reduced in a stepwise manner from stable NREM, to tonic REM to phasic REM sleep to a similar extent in OSA and healthy individuals of both genders.

116 citations

Journal ArticleDOI
TL;DR: A relative deficiency of REM sleep may indicate an abnormality in neural organization in young children with autism that is not directly associated with or related to inherent intellectual disability but may serve as a window into understanding core neurotransmitter abnormalities unique to this disorder.
Abstract: Objective To compare objective polysomnographic parameters between 3 cohorts: children with autism, typical development, and developmental delay without autism. Design Overnight polysomnographic recordings were scored for sleep architecture according to American Academy of Sleep Medicine criteria by a board-certified sleep medicine specialist blind to diagnosis for studies collected between July 2006 and September 2009. Setting Subjects were evaluated in the pediatric ward in the Clinical Research Center of the National Institutes of Health. Participants First 60 consecutive children with autism, 15 with typical development, and 13 with developmental delay matched for nonverbal IQ to the autism group, ranging in age from 2 to 13 years, selected without regard to the presence or absence of sleep problem behavior. Main Outcome Measures Total sleep time, latencies to non–rapid eye movement (REM) and REM sleep, and percentages of total sleep time for stages 1 and 2 sleep, slow-wave sleep, and REM sleep. Results There were no differences between the typical vs developmental delay groups. Comparison of children with autism vs typical children revealed shorter total sleep time ( P = .004), greater slow-wave sleep percentage ( P = .001), and much smaller REM sleep percentage (14.5% vs 22.6%; P P = .001), greater stage 1 sleep percentage ( P P P Conclusion A relative deficiency of REM sleep may indicate an abnormality in neural organization in young children with autism that is not directly associated with or related to inherent intellectual disability but may serve as a window into understanding core neurotransmitter abnormalities unique to this disorder.

116 citations

Journal ArticleDOI
TL;DR: Results of heart rate variability (HRV) analysis have revealed higher parasympathetic tone during normal non-REMS and a shift toward sympathetic predominance during normal REMS and the potential of HRV analysis to explore the sleeping brain, and the implications for psychiatric disorders.
Abstract: Sleep is divided into two main sleep stages: (1) non-rapid eye movement sleep (non-REMS), characterized among others by reduced global brain activity; and (2) rapid eye movement sleep (REMS), characterized by global brain activity similar to that of wakefulness. Results of heart rate variability (HRV) analysis, which is widely used to explore autonomic modulation, have revealed higher parasympathetic tone during normal non-REMS and a shift toward sympathetic predominance during normal REMS. Moreover, HRV analysis combined with brain imaging has identified close connectivity between autonomic cardiac modulation and activity in brain areas such as the amygdala and insular cortex during REMS, but no connectivity between brain and cardiac activity during non-REMS. There is also some evidence for an association between HRV and dream intensity and emotionality. Following some technical considerations, this review addresses how brain activity during sleep contributes to changes in autonomic cardiac activity, organized into three parts: (1) the knowledge on autonomic cardiac control, (2) differences in brain and autonomic activity between non-REMS and REMS, and (3) the potential of HRV analysis to explore the sleeping brain, and the implications for psychiatric disorders.

116 citations

Journal ArticleDOI
TL;DR: The subpopulation of cholinoceptive PRF neurons accelerated during both spontaneous andcarbachol-induced REM sleep is most likely to account for REM sleep triggering by carbachol, and the PRF neuron found to be decelerated by carbACHol displayed under control conditions, the accelerated discharge pattern during REM sleep which is typical of PRf neurons.

116 citations

Journal ArticleDOI
TL;DR: The present study has demonstrated that the sleep‐promoting potency of 2‐[p‐(2‐carboxyethyl)phenethylamino]‐5′‐N‐ethylcarboxamido adenosine (CGS21680), a selective agonist for theAdenosine A2A receptor, varies depending on the location of the administration.
Abstract: The present study has demonstrated that the sleep-promoting potency of 2-[p-(2-carboxyethyl)phenethylamino]-5′-N-ethylcarboxamido adenosine (CGS21680), a selective agonist for the adenosine A2A receptor, varies depending on the location of the administration. CGS21680 was continuously administered to rats through a chronically implanted cannula for 6 h during their active phase. The tip of the cannula was located in the subarachnoid space or the brain ventricle neighbouring the established brain areas implicated in the regulation of sleep–wake phenomena, i.e. rostral basal forebrain, medial preoptic area, lateral preoptic area, posterior hypothalamus, and dorsal tegmentum of the pons and medulla. At an infusion rate of 2.0 pmol/min, the magnitude of increase in non-rapid eye movement sleep varied from 14 min (a 15% increase) to 96 min (a 103% increase), and those of rapid eye movement sleep varied from 6 min (a 40% increase) to 28 min (a 264% increase) from the respective baseline values. The largest increases in both types of sleep occurred when CGS21680 was administered to the subarachnoid space underlying the rostral basal forebrain. These findings were interpreted to mean that the major, if not the only, site responsible for the CGS21680-inducing sleep was located in or near the rostral basal forebrain. This interpretation was supported by the findings that the administration of CGS21680 to the rostral basal forebrain produced predominant expression of Fos within the shell of the nucleus accumbens and the medial portion of the olfactory tubercle, and that the microdialysis perfusion of CGS21680 into the shell of the nucleus accumbens also exhibited a sleep-promoting effect.

116 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202353
2022115
2021116
2020107
201995
201883