ArticleSleep2016
RGS Proteins and Gαi2 Modulate Sleep, Wakefulness, and Disruption of Sleep/ Wake States after Isoflurane and Sevoflurane Anesthesia.
Article in Sleep, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Esketamine improves postoperative sleep quality in thoracic surgery patients with preoperative sleep disturbance: a randomized controlled trial.Frontiers in pharmacology · 2026Trial
- Therapeutic Potential of Anesthesiology for Sleep Disorders in the Perioperative Period.Current neuropharmacology · 2026Review
- Anatomical Substrates of Rapid Eye Movement Sleep Rebound in a Rodent Model of Post-sevoflurane Sleep Disruption.Anesthesiology · 2024Article
- Neurotransmitter networks in mouse prefrontal cortex are reconfigured by isoflurane anesthesia.Journal of neurophysiology · 2020Article
- Genome-Wide Screen for Genes Involved inG3 (Bethesda, Md.) · 2017Article
- Ketamine and propofol have opposite effects on postanesthetic sleep architecture in rats: relevance to the endogenous sleep-wakefulness substances orexin and melanin-concentrating hormone.Journal of anesthesia · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
STUDY
objectivesThis study tested the hypothesis that Regulators of G protein Signaling (RGS) proteins contribute to the regulation of wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep, and to sleep disruption caused by volatile anesthetics.
methodsThe three groups used in this study included wild-type (WT; n = 7) mice and knock-in mice that were heterozygous (+/GS; n = 7) or homozygous (GS/GS; n = 7) for an RGS-insensitive allele that causes prolonged Gαi2 signaling. Mice were implanted with electrodes for recording sleep and conditioned for 1 week or more to sleep in the laboratory. Using within and between groups designs, 24-h recordings of wakefulness, NREM sleep, and REM sleep were compared across three interventions: (1) baseline (control) and after 3 h of being anesthetized with (2) isoflurane or (3) sevoflurane.
resultsBaseline recordings during the light phase revealed that relative to WT mice, homozygous RGS-insensitive (GS/GS) mice exhibit significantly increased wakefulness and decreased NREM and REM sleep. During the dark phase, these state-specific differences remained significant but reversed direction of change. After cessation of isoflurane and sevoflurane anesthesia there was a long-lasting and significant disruption of sleep and wakefulness. The durations of average episodes of wakefulness, NREM sleep, and REM sleep were significantly altered as a function of genotype and isoflurane and sevoflurane anesthesia.
conclusionsRGS proteins and Gαi2 play a significant role in regulating states of wakefulness, NREM sleep, and REM sleep. Genotype-specific differences demonstrate that RGS proteins modulate sleep disruption caused by isoflurane and sevoflurane anesthesia. The results also support the conclusion that isoflurane and sevoflurane anesthesia do not satisfy the homeostatic drive for sleep.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.