Disease relevance of REM1

• 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].
• Letter: REM sleep and cardiac arrhythmias [3].
• Absence of REM and altered NREM sleep in patients with spinocerebellar degeneration and slow saccades [4].
• In 100 consecutive adults who came to a sleep disorders center complaining of repeated nocturnal injury, polysomnographic study identified five disorders: night terrors/sleepwalking (N = 54), REM sleep behavior disorder (N = 36), dissociative disorders (N = 7), nocturnal seizures (N = 2), and sleep apnea (N = 1) [5].

Psychiatry related information on REM1

• Letter: Narcolepsy: REM sleep suppression by L-dopa [6].
• We propose that the function of dream sleep (more properly rapid-eye movement or REM sleep) is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex [7].
• Humans with pharmacological and brain lesion-induced suppression of REM sleep do not show memory deficits, and other human sleep-learning studies have not produced consistent results [8].
• Spontaneous brain oscillations during states of vigilance are associated with neuronal plasticity due to rhythmic spike bursts and spike trains fired by thalamic and neocortical neurons during low-frequency rhythms that characterize slow-wave sleep and fast rhythms occurring during waking and REM sleep [9].
• The main clinical features of narcolepsy, excessive daytime sleepiness and symptoms of abnormal REM sleep (cataplexy, sleep paralysis, hypnagogic hallucinations) are currently treated using amphetamine-like compounds or modafinil and antidepressants [10].

High impact information on REM1

• It has been hypothesized that REM (rapid eye movement) sleep has an important role in memory consolidation [8].
• Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density [11].
• Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism [11].
• A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms [11].
• We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep [12].

Chemical compound and disease context of REM1

• Acetylcholine and the regulation of REM sleep: basic mechanisms and clinical implications for affective illness and narcolepsy [13].
• In this view the level of extracellular serotonin would be consistent with the pattern of discharge of the DRN serotonergic neurons which show the highest firing rate during W, followed by a decrease in slow wave sleep and by virtual electrical silence during REM sleep [14].
• With one exception (pimozide), all the drugs that suppressed cataplexy are known to be potent suppressors of REM sleep [15].
• The biological profile of an anergic episode of bipolar depression did not include a shorter than normal mean REM latency, poor sleep continuity, or abnormally low amounts of stages 3 and 4 sleep, and only three (13%) of 23 patients manifested cortisol nonsuppression [16].
• Two biological markers--shortened REM latency and nonsuppression on the dexamethasone suppression test--suggested that both patients may have had an underlying affective disorder [17].

Biological context of REM1

• A new long terminal repeat (LTR) retrotransposon, named REM1, has been identified in the green alga Chlamydomonas reinhardtii [18].
• Heart rates were counted for a 40-min period following the end of REM1 [19].
• 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 [20].
• We address this issue first on the cellular level, considering how activation of T-type Ca(2+) channels in nonREM sleep may promote either long-term depression or long-term potentiation, as well as how cellular events of REM sleep may influence these processes [21].
• A cDNA library was constructed from a homozygous B lymphoblastoid cell line (REM) obtained from an individual of a long isolated American Indian tribe, the Warao [22].

Anatomical context of REM1

• We report that Ges (GTPase regulating endothelial cell sprouting), a human RGK protein expressed in the endothelium, functions as a potent morphogenic switch in endothelial cells (ECs) [23].
• (2) As well as a role in the mediation of REM sleep, cholinergic PPTg neurons have an important role in the waking state, providing feedback into the thalamus and striatum [24].
• This observation suggests that CWS (1) can represent a distinct and isolated neuropsychological manifestation of deep occipital lobe damage, and (2) may occur in the absence of detectable REM sleep abnormalities [25].
• Sequence of a DQ beta clone from the DRw 15-Dw 22 cell line REM [26].
• REM sleep and amygdala [27].

Associations of REM1 with chemical compounds

• Analysis of sleep effects of flurazepam hydrochloride on four normal subjects confirmed that this drug substantially suppresses both REM and stage 4 sleep [28].
• This suggests that during waking serotonin may complement the action of noradrenaline and acetylcholine in promoting cortical responsiveness and participate to the inhibition of REM-sleep effector neurons in the brainstem (inhibitory role on REM sleep) [14].
• It is a multidomain protein composed of several recognizable sequence motifs in the following order (NH(2) to COOH): pleckstrin homology (PH), coiled-coil, ilimaquinone (IQ), Dbl homology (DH), PH, REM (Ras exchanger motif), PEST/destruction box, Cdc25 [29].
• In narcoleptics, impaired control of sleep-wake and REM mechanisms is attentuated by methylphenidate [30].
• However, total times in deeper stages of non-rapid eye movement (non-REM; e.g., delta sleep) and REM sleep were not significantly affected by SCN lesions [31].

Analytical, diagnostic and therapeutic context of REM1

• The absence of REM sleep was demonstrated by polysomnography in two patients [32].
• The role of the endogenous circadian pacemaker in the timing of the sleep-wake cycle and the regulation of the internal structure of sleep, including REM sleep, EEG slow-wave (0.75-4.5 Hz) and sleep spindle activity (12.75-15.0 Hz) was investigated [33].
• By contrast, slow wave sleep and tonic REM measures, including reduced REM latency, were unchanged after treatment [34].
• MEASUREMENTS AND MAIN RESULTS: Microdialysis perfusion of the alpha(1) receptor antagonist terazosin into the HMN significantly decreased GG activity in wakefulness and nonrapid eye movement (non-REM) sleep but not REM sleep [35].
• REM sleep abnormalities in a new animal model of endogenous depression [36].

References