Topic
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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TL;DR: The cholinergic agonist carbachol was injected into the pontine Pb area where PGO bursting cells have been recorded and this experimental preparation is a useful model for the study of the electrophysiology and functional significance of PGO wave and REM sleep generation.
Abstract: The cholinergic agonist carbachol was injected into the pontine Pb area where PGO bursting cells have been recorded. When microinjections were localized to the ventrolateral aspect of the caudal Pb nucleus near aggregates of ChAT immunolabeled cholinergic neurons, carbachol produced an immediate onset of state-independent PGO waves in the ipsilateral LGB. These state-independent PGO waves persisted for 3-4 days. After the first 24 hrs PGO wave activity increasingly became associated with REM sleep and with REM transitional SP sleep as both of these PGO-related states increased in amount to 3-4 times baseline levels. The increase in amount of PGO-related states peaked on days 2-4 following one carbachol injection and persisted for 10-12 days. These results suggest a two stage process: stage one, PGO enhancement, is the direct consequence of the membrane activation of cholinoceptive PGO burst neurons by carbachol; stage two, REM enhancement, is the consequence of metabolic activation of endogenous cholinergic neurons. This experimental preparation is a useful model for the study of the electrophysiology and functional significance of PGO wave and REM sleep generation.
63 citations
TL;DR: The results suggest that initial decreases and subsequent increases in sleep time are related to putative differences in the intensity of environmental novelty and to previously described strain differences in anxiety.
63 citations
TL;DR: Data show that gaboxadol counteracts the disrupting effects of a nap on subsequent sleep and suggest that, in addition to promoting deep sleep and sleep maintenance, gab oxadol is able to facilitate sleep initiation and thus, exhibits significant hypnotic actions under conditions in which sleep quality is experimentally reduced.
Abstract: Rationale: Previous studies demonstrated that gaboxadol, a selective GABAA agonist, increases both non-REM sleep and EEG delta activity within non-REM sleep in rats and slow wave sleep (SWS) as well as low-frequency activity in the EEG within non-REM sleep in healthy humans under normal conditions. Objective: Because the hypnotic actions of drugs may be more readily demonstrated under conditions of poor sleep quality, we investigated the influence of gaboxadol on postnap sleep. Methods: In a randomized, placebo-controlled cross-over study using a late afternoon nap model, we assessed the effects of a single oral dose of 20 mg gaboxadol on disturbed nighttime sleep in young, healthy subjects. Results: Comparisons of visually scored sleep parameters between baseline and placebo postnap nights showed that the nap prolonged sleep latency, decreased total sleep time and SWS and attenuated delta, theta and alpha activity in the EEG within non-REM sleep. Compared with the placebo postnap night, gaboxadol tended to shorten sleep latency, significantly decreased intermittent wakefulness, increased total sleep time and SWS and enhanced delta and theta activity in the non-REM EEG. Furthermore, gaboxadol increased subjective sleep quality. Conclusions: These data show that gaboxadol counteracts the disrupting effects of a nap on subsequent sleep and suggest that, in addition to promoting deep sleep and sleep maintenance, gaboxadol is able to facilitate sleep initiation and thus, exhibits significant hypnotic actions under conditions in which sleep quality is experimentally reduced.
63 citations
TL;DR: A replication‐defective herpes simplex virus‐1 amplicon‐based vector was constructed to transfer the gene for mouse prepro‐orexin into mice with a genetic deletion of the orexin gene, and the incidence of cataplexy declined, indicating that narcoleptic sleep–wake behavior in orexIn KO mice can be improved by targeted gene transfer.
Abstract: Gene transfer has proven to be an effective neurobiological tool in a number of neurodegenerative diseases, but it is not known if it can correct a sleep disorder. Narcolepsy is a neurodegenerative sleep disorder linked to the loss of neurons containing the neuropeptide orexin, also known as hypocretin. Here, a replication-defective herpes simplex virus-1 amplicon-based vector was constructed to transfer the gene for mouse prepro-orexin into mice with a genetic deletion of the orexin gene. After in vitro tests confirmed successful gene transfer into cells, the gene vector was delivered to the lateral hypothalamus of orexin knockout (KO) mice where the orexin peptide was robustly expressed in the somata and processes of numerous neurons, and the peptide product was detected in the cerebrospinal fluid. During the 4-day life-span of the vector the incidence of cataplexy declined by 60%, and the levels of rapid eye movement sleep during the second half of the night were similar to levels in wild-type mice, indicating that narcoleptic sleep-wake behavior in orexin KO mice can be improved by targeted gene transfer.
63 citations
TL;DR: The results suggest that aspects of sleep architecture can be adjusted to the prevailing risk of predation, and mammals should selectively reduce deep SWS and REM sleep following an increase in the risk ofpredation.
63 citations