Disease relevance of Sleep, REM

• In Parkinson's disease, the additional loss of pedunculopontine cholinergic neurones, which control REM (rapid eye movement) sleep or dreaming, is likely to contribute to REM abnormalities, which also occur in DLB [1].
• Low-flow oxygen significantly reduced the duration of Cheyne-Stokes respiration (50.7% +/- 12.0% to 24.2% +/- 5.4% total sleep time), mainly during stage 1 NREM (non-rapid eye movement) sleep (21.3% +/- 7.1% to 6.7% +/- 2.3% total sleep time) with no significant change during stage 2 sleep, slow-wave sleep, or REM (rapid eye movement) sleep [2].
• During the acute phase of the illness, the patients had abnormally short rapid eye movement sleep latencies, hypercortisolism, early timing of the nadirs of the ACTH-cortisol rhythms, and shorter nocturnal periods of quiescent cortisol secretion [3].
• Since acetylcholine is the putative brain stem transmitter substance involved in the maintenance of REM sleep, our findings suggest a disturbed central mechanism of acetylcholine in myasthenia gravis [4].
• Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep [5].

Psychiatry related information on Sleep, REM

• Acetylcholine (ACh) plays a key role in the transitions between the different phases of sleep: Slow-wave sleep requires low ACh concentrations in the brain, whereas rapid-eye-movement (REM) sleep is associated with high levels of ACh [6].
• C-fos expression in orexin neurons, an indicator of neuronal activation, is positively correlated with wakefulness and negatively correlated with rapid eye movement (REM) and non-REM sleep states [7].
• Flurazepam has relatively minor effects upon rapid eye movement (REM) sleep and does not lead to REM rebound; this may reduce the likelihood of drug dependence [8].
• These results indicate that PGE2 modifies cataplexy through a central effect and suggest that this prostaglandin may play a role in rapid-eye-movement sleep regulation [9].
• The therapeutic potential of thyrotropin-releasing hormone (TRH) and TRH analogs in narcolepsy, a sleep disorder characterized by abnormal rapid eye movement (REM) sleep and daytime sleepiness, was examined using the canine model [10].

High impact information on Sleep, REM

• Here we show that a deficiency in short-chain acyl-coenzyme A dehydrogenase (encoded by Acads) in mice causes a marked slowing in theta frequency during paradoxical sleep only [11].
• Also, these phases of sleep are differentially sensitive to a number of endogenous neuropeptides and cytokines, including somatostatin, which has been shown to increase REM sleep without significantly affecting other phases [6].
• It has been hypothesized that REM (rapid eye movement) sleep has an important role in memory consolidation [12].
• Microinjection of this pharmacologically active probe into the gigantocellular field of the cat pontine brain stem caused the awake cats to fall into rapid movement (REM) sleep indistinguishable from that produced by free carbachol [13].
• Arecoline, a cholinergic muscarinic receptor agonist, induced rapid eye movement sleep significantly more rapidly in patients with primary affective illness in remission than in normal control subjects matched for age and sex [14].

Chemical compound and disease context of Sleep, REM

• Newborn infants, chronically exposed in utero to low doses of methadone with or without concomitant heroin, display more rapid eye movement sleep and less quiet sleep than control infants, while babies fetally exposed to both opiates and nonopiates have less organization of sleep states [15].
• A trend for an association between lower amounts of REM sleep and higher evening cortisol concentrations independent of age was detected (P<.10) [16].
• In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states [17].
• The dopamine agonist significantly decreased rapid eye movement (REM) sleep and percent REM sleep and increased REM latency [18].
• Physostigmine, an anticholinesterase that increases the action of brain acetylcholine, induces rapid eye movement (REM) sleep in normal humans [19].
• In the discussion, arguments supporting the requirement for a given level of noradrenaline for REM sleep occurrence are presented [20].

Biological context of Sleep, REM

• Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm [21].
• We conclude that endogenous elevations of circulating DSIP may be associated with suppression of slow wave and rapid eye movement sleep, and that the circadian rhythm of this peptide is coupled directly or indirectly to that of body temperature [22].
• REM sleep was associated with a decrease in cortisol secretory rates preceding REM sleep onset, whereas the LF/HF ratio and rRR remained high [23].
• Methadone is equipotent to morphine in its increase of wakefulness, drowsiness, muscle tension, shifts in sleep-waking state, and latency to rapid eye movement sleep (REMS) and its decrease of sleep efficiency, delta sleep, and REMS [24].
• RESULTS--The mean (SD) increase in blood pressure (delta MBP) during apnoeic episodes was 42.1 (17.3) mm Hg during rapid eye movement (REM) sleep and 31.9 (12.5) mm Hg during non-REM sleep [25].

Anatomical context of Sleep, REM

• Carbachol enhances rapid eye movement (REM) sleep when microinjected into the pontine reticular formation of the cat and rat [26].
• Microdialysis perfusion of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) in the dorsal raphe nucleus decreases serotonin release and increases rapid eye movement sleep in the freely moving cat [27].
• Simultaneous injection of carbachol into the pons and basal forebrain enhanced REM sleep, but the magnitude of this enhancement was significantly less than the increase in REM sleep evoked by carbachol injection into the pons alone [28].
• This approach indicates that LTH is modulated by NMDA receptors, requires polysome aggregation and protein synthesis, a functioning neocortex and both slow wave and paradoxical sleep [29].
• We compared blood-brain barrier (BBB) permeability to glucose between quiet wakefulness and rapid-eye-movement (REM) sleep to assess whether changes in BBB permeability play a role in coupling glucose supply to the physiologic metabolic needs of the brain [30].

Gene context of Sleep, REM

• In contrast, OX2R(-/-) mice are only mildly affected with cataplexy-like attacks of REM sleep, whereas orexin(-/-) mice are severely affected [31].
• Hcrt cells are silent in slow wave sleep and tonic periods of REM sleep, with occasional burst discharge in phasic REM [32].
• Altogether, these data indicate that 5-HT1B receptors participate in the regulation of paradoxical sleep in the mouse [33].
• After SRIF administration, total sleep time and rapid eye movement (REM) sleep decreased significantly, and more time was spent awake in the first sleep cycle, suggesting that SRIF induces sleep deterioration in the elderly [34].
• Changes in hypothalamic corticotropin-releasing hormone, neuropeptide Y, and proopiomelanocortin gene expression during chronic rapid eye movement sleep deprivation of rats [35].

Analytical, diagnostic and therapeutic context of Sleep, REM

• We studied the relation between REM sleep suppression and antidepressant response and the effect of phenelzine therapy on sleep EEG power spectra [36].
• DESIGN: Subjects completed electroencephalographic sleep and regional cerebral glucose metabolism assessments during both waking and REM sleep using [(18)F]fluoro-2-deoxy-D-glucose positron emission tomography [37].
• To assess the association of the overall amount of rapid eye movement (REM) sleep and the activities of the hypothalamic-pituitary-adrenal axis and sympathetic system, we performed polysomnography and measured 24-h urinary free cortisol and catecholamine excretion in 21 healthy adults [38].
• After treatment, rapid eye movement sleep latencies were lengthened, and cortisol levels returned to normal due to a decrease in the magnitude of episodic pulses [3].
• Melatonin in patients with reduced REM sleep duration: two randomized controlled trials [39].

References