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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
TL;DR: An MCH, CART, and Fos triple immunolabeling study in PS hypersomniac rats showed that the MCH neurons activated during PS are part of both subpopulations since they found CART and non‐CART MCH‐activated neurons.
Abstract: Although the main nodes of the neuronal network that regulate paradoxical sleep (PS), also called rapid eye movement sleep, have been identified in rodents, it still needs to be more thoroughly described. We have recently shown that 58% of a hypothalamic neuronal population, the melanin-concentrating hormone (MCH) neurons, are activated after a PS hypersomnia and that MCH, when injected intracerebroventricularly, induces a dose-dependent increase in PS. This suggests that MCH plays a role in PS regulation. Two subpopulations of MCH neurons have been distinguished neurochemically, one that coexpresses cocaine and amphetamine-regulated transcript (CART) and sends ascending projections to the septum and the hippocampus, the other, the non-CART MCH neurons, send descending projections to the lower brainstem and the spinal cord. In order to better characterize the PS-activated MCH neurons it is interesting to determine whether they belong to the first, the second, or both subgroups. We therefore undertook an MCH, CART, and Fos triple immunolabeling study in PS hypersomniac rats. We showed that the MCH neurons activated during PS are part of both subpopulations since we found CART and non-CART MCH-activated neurons. Based on these results and the literature, we propose that MCH could be involved in memory processes and in the inhibition of muscle tone during PS. J. Comp. Neurol. 505:147–157, 2007. © 2007 Wiley-Liss, Inc.

80 citations

Journal ArticleDOI
TL;DR: It is suggested that sleep stages play a minor role in the variance of SMR among subjects, however, the duration of sleep may contribute to the variability of 24-h energy expenditure.
Abstract: Differences in sleeping metabolic rate (SMR) among subjects may be related to different levels of energy expenditure associated with sleep stages. The relationship between energy expenditure and sleep stages was investigated overnight in 29 subjects (14 Caucasians and 15 Pima Indians, 18 males and 11 females; mean +/- SD, 31 +/- 7 yr, 83 +/- 26 kg, 27 +/- 11% fat). Sleep stages were determined by electroencephalogram recording, whereas energy expenditure was measured in a 1,000-liter Plexiglas sleep box constructed around a bed as a fast-response open-circuit indirect calorimeter. Eighty-five percent of the interindividual variability in SMR was explained by differences in fat-free mass, fat mass, age, sex, and race (r2 = 0.85). The intra-individual variance in SMR over time was related to sleep stages and to clock time. Within subjects, SMR in stage 3 was significantly lower than in stage 2 (-39 +/- 18 kcal/day; P < 0.05) and rapid eye movement sleep (-51 +/- 23 kcal/day; P < 0.05). Also, sleep stages were associated with different respiratory quotients. Because sleep stages are associated with only small differences in energy metabolism, our results suggest that sleep stages play a minor role in the variance of SMR among subjects. However, the duration of sleep may contribute to the variability of 24-h energy expenditure.

80 citations

Journal ArticleDOI
D. A. Sack1, W. Duncan1, N. E. Rosenthal1, W. E. Mendelson1, T. A. Wehr1 
TL;DR: There was a significant negative correlation between response to PSD and sleep duration, and in particular, REMSleep duration, in the late sleep deprivation situation, and the amount and timing of sleep appear to be factors in the response toPSD.
Abstract: — The antidepressant response to partial sleep deprivation early in the night (PSD-E) was compared with the response to partial sleep deprivation late in the night (PSD-L) in 16 drug-free depressed inpatients using a balanced order crossover design. PSD-L had a significantly greater antidepressant effect that PSD-E. The response to PSD-L was sustained and enhanced by a second night of treatment. Patients had significantly shorter sleep durations and reduced REM sleep on PSD-L that did not occur in the PSD-E situation. There was a significant negative correlation between response to PSD and sleep duration, and in particular, REM sleep duration, in the late sleep deprivation situation. Thus, the amount and timing of sleep appear to be factors in the response to PSD, but additional studies are needed to evaluate the relative importance of these parameters.

80 citations

Journal ArticleDOI
TL;DR: It is speculated that patients with Rett syndrome have normal breathing during non-rapid eye movement (NREM) sleep, and that the disordered breathing seen during wakefulness is due to an abnormality of the cortical influence on ventilation.

80 citations

Journal ArticleDOI
TL;DR: It is found that REM latency was significantly decreased in Addison's patients when receiving hydrocortisone at bedtime, whereas REM sleep time was increased, and cortisol plays a positive, permissive role in REM sleep regulation and may help to consolidate sleep.
Abstract: There is a well described temporal relation between hormonal secretion and sleep phase, with hormones of the hypothalamicpituitary-adrenal (HPA) axis possibly playing a role in determining entry into and duration of different sleep stages. In this study sleep features were studied in primary Addison’s patients with undetectable levels of cortisol treated in a double blind, randomized, cross-over fashion with either hydrocortisone or placebo supplementation. We found that REM latency was significantly decreased in Addison’s patients when receiving hydrocortisone at bedtime, whereas REM sleep time was increased. There was a trend toward an increase in the percentage of time in REM sleep and the number of REM sleep episodes. Waking time after sleep onset was increased, whereas no differences were observed between the two conditions when total sleep time or specific non-REM sleep parameters were evaluated. Our results suggest that in Addison’s patients, cortisol plays a positive, permissive role in REM sleep regulation and may help to consolidate sleep. These effects may be mediated either directly by the central effects of glucocorticoids and/or indirectly through CRH and/or ACTH. (J Clin Endocrinol Metab 85: 4201‐ 4206, 2000)

80 citations


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