Behavioral Response and Transmitter Release During Atonia Elicited by Medial Medullary Stimulation

Activation of the medial medulla is responsible for rapid eye movement (REM) sleep atonia and cataplexy. Dysfunction can cause REM sleep behavior disorder and other motor pathologies. Here we report the behavioral effects of stimulation of the nucleus gigantocellularis (NGC) and nucleus magnocellularis (NMC) in unrestrained cats. In waking, 62% of the medial medullary stimulation sites suppressed muscle tone. In contrast, stimulation at all sites, including sites where stimulation produced no change or increased muscle tone in waking, produced decreased muscle tone during slow-wave sleep. In the decerebrate cat electrical stimulation of the NGC increased glycine and decreased norepinephrine (NE) release in the lumbar ventral horn, with no change in γ-aminobutyric acid (GABA) or serotonin (5-HT) release. Stimulation of the NMC increased both glycine and GABA release and also decreased both NE and 5-HT release in the ventral horn. Glutamate levels in the ventral horn were not changed by either NGC or NMC stimulation. We conclude that NGC and NMC play neurochemically distinct but synergistic roles in the modulation of motor activity across the sleep–wake cycle via a combination of increased release of glycine and GABA and decreased release of 5-HT and NE. Stimulation of the medial medulla that elicited muscle tone suppression also triggered rapid eye movements, but never produced the phasic twitches that characterize REM sleep, indicating that the twitching and rapid eye movement generators of REM sleep have separate brain stem substrates

Association between Glucose Metabolism and Sleep-disordered Breathing during REM Sleep

Rationale: Sleep-disordered breathing (SDB) has been associated with impaired glucose metabolism. It is possible that the association between SDB and glucose metabolism is distinct for non-REM versus REM sleep because of differences in sleep-state–dependent sympathetic activation and/or degree of hypoxemia. Objectives: To characterize the association between REM-related SDB, glucose intolerance, and insulin resistance in a community-based sample. Methods: A cross-sectional analysis that included 3,310 participants from the Sleep Heart Health Study was undertaken (53% female; mean age, 66.1 yr). Full montage home-polysomnography and fasting glucose were available on all participants. SDB severity during REM and non-REM sleep was quantified using the apnea–hypopnea index in REM (AHI(REM)) and non-REM sleep (AHI(NREM)), respectively. Fasting and 2-hour post-challenge glucose levels were assessed during a glucose tolerance test (n = 2,264). The homeostatic model assessment index for insulin resistance (HOMA-IR) was calculated (n = 1,543). Linear regression was used to assess the associations of AHI(REM) and AHI(NREM) with fasting and post-prandial glucose levels and HOMA-IR. Measurements and Main Results: AHI(REM) and AHI(NREM) were associated with fasting glycemia, post-prandial glucose levels, and HOMA-IR in models that adjusted for age, sex, race, and site. However, with additional adjustment for body mass index, waist circumference, and sleep duration, AHI(REM) was only associated with HOMA-IR (β = 0.04; 95% CI, 0.1–0.07; P = 0.01), whereas AHI(NREM) was only associated with fasting (β = 0.93; 95% CI, 0.14–1.72; P = 0.02) and post-prandial glucose levels (β = 3.0; 95% CI, 0.5–5.5; P = 0.02). Conclusions: AHI(REM) is associated with insulin resistance but not with fasting glycemia or glucose intolerance