Disease relevance of Sleep

• Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL [1].
• A high frequency of central apneas during light slow-wave sleep was linked to the male sex; a high frequency of central apneas during REM sleep was linked to the amount of REM sleep [2].
• Our own experience suggests that the Landau-Kleffner syndrome and epilepsy with continuous spike-wave activity in slow-wave sleep cannot be clearly differentiated [3].
• In addition, the behavioural and ECoG slow-wave sleep observed after intraperitoneal administration of clonidine (0.2 mumol kg-1) was significantly reduced by prior (3 days) microinfusion of pertussis toxin into the locus coeruleus [4].
• Bruxism episodes were equally distributed between non-REM and REM sleep, but were more frequent in stages 1 and 2 (p < 0.0001) than in slow-wave sleep [5].

Psychiatry related information on Sleep

• We have also found that the concentration of dopamine increases in the hippocampus during slow-wave sleep, and suggest that this may be related to the subsequent appearance of paradoxical sleep [6].
• In vivo microdialysis measurements in freely behaving cats showed that adenosine extracellular concentrations in the basal forebrain cholinergic region increased during spontaneous wakefulness as contrasted with slow wave sleep; exhibited progressive increases during sustained, prolonged wakefulness; and declined slowly during recovery sleep [7].
• Central administration of NPS increases locomotor activity in mice and decreases paradoxical (REM) sleep and slow wave sleep in rats [8].
• Nocturnal plasma melatonin concentrations were unrelated to sleep stages, whereas secretion of GH was temporally related to slow wave sleep [9].
• CONCLUSIONS: Alcohol dependence compromises the augmentation of slow wave sleep and delta power seen in healthy adults following sleep deprivation [10].

High impact information on Sleep

• Flurazepam effects on slow-wave sleep: stage 4 suppressed but number of delta waves constant [11].
• We have found that the metabolism of 5-hydroxytryptamine increases in the hippocampus and that the metabolism of dopamine decreases in the striatum and thalamus during slow-wave sleep, and we suggest that these changes are related to this stage of sleep [6].
• Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men [12].
• Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<.001) [12].
• The effects of several analogs of MDP on rabbit slow-wave sleep are presented and these results are compared to the dose-response relationship for MDP [13].

Chemical compound and disease context of Sleep

• Simultaneous stimulation of slow-wave sleep and growth hormone secretion by gamma-hydroxybutyrate in normal young Men [14].
• Reversal of slow-wave sleep by benzodiazepine antagonist Ro 15-1788 [15].
• However, prostaglandin D2 at as little as 60 fmol/min caused a significant amount of excess slow wave sleep as compared with the control level during saline infusion [16].
• Low acetylcholine during slow-wave sleep is critical for declarative memory consolidation [17].
• Although prostaglandin F2 alpha (600 fmol/min) increased the amount of slow wave sleep, its activity was less than that of the same amount of prostaglandin D2 [16].

Biological context of Sleep

• 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 [18].
• During waking, components in event related potentials (ERP) are moderate in amplitude, while during slow wave sleep larger waves are visible [19].
• The number of eye movements (> 75 microV) and the amplitude of EOG and EMG activity increased significantly on treatment in REM, stages 1, 2, and slow-wave sleep [20].
• Here we show that systemic administration of oleamide (10 and 20 mg/kg) in rats increased slow-wave sleep 2, without affecting blood pressure and heart rate [21].
• These neurochemical and drug interaction data raise the possibility that 5-hydroxytryptamine is involved in the control of paradoxical rather than slow-wave sleep in the rat [22].

Anatomical context of Sleep

• Independence of glutamate response modulation from changes of baseline firing was also observed in a different data set obtained from 19 Purkinje cells which were recorded during a continuous slow-wave sleep period that allowed several consecutive drug applications [23].
• We used in vivo microdialysis coupled with polygraphic recording to monitor 5-hydroxytryptamine levels in the dorsal raphe nucleus and frontal cortex across waking, slow-wave sleep and rapid eye-movement sleep [24].
• 2 Behavioural and electrocortical slow wave sleep were induced by clonidine infused into IIIrd cerebral ventricle, the hypothalamus or intravenously [25].
• Bilateral injections of alpha-FMH (50 micrograms/1 microliter) into the ventrolateral posterior hypothalamus, where histamine immunoreactive neurones have been recently identified, resulted in a significant decrease in wakefulness and increase in deep slow wave sleep [26].
• Bilateral injections of m-chlorophenylbiguanide into the nucleus accumbens of the control and the vehicle-infused animals significantly increased waking and reduced slow wave sleep [27].

Gene context of Sleep

• In young normal subjects, GHRH stimulates slow-wave sleep and growth hormone secretion but inhibits cortisol release, whereas CRH has the opposite effect [28].
• Hexarelin decreases slow-wave sleep and stimulates the secretion of GH, ACTH, cortisol and prolactin during sleep in healthy volunteers [29].
• Similar to GH-releasing hormone (GHRH) ghrelin promotes slow-wave sleep in humans, whereas GH-releasing peptide-6 (GHRP-6) enhances stage 2 nonrapid-eye movement sleep (NREMS) [29].
• The systemic effects of IL-1 include fever, increased circulating neutrophils, hepatic acute phase proteins, slow wave sleep, elevated insulin levels and hypotension [30].
• Besides GHRH, ghrelin and galanin enhance slow wave sleep [31].

Analytical, diagnostic and therapeutic context of Sleep

• The usual increase in plasma cortisol in the early morning was completely suppressed in all five subjects given cyproheptadine infusions from 4:00 to 7:00 a.m. The intravenous infusion of cyproheptadine increased slow wave sleep, although the time from sleep onset to the first occurrence of slow wave sleep was not affected [32].
• By contrast, slow wave sleep and tonic REM measures, including reduced REM latency, were unchanged after treatment [33].
• Based upon spectral analysis the EEG was classified into three categories: awake, slow-wave sleep (SWS), and rapid eye movement sleep (REM) [34].
• Finally, REM and slow wave sleep occurred together during only 27 of 910 bedrest episodes [35].
• Microinjections of mepyramine alone (120 micrograms in 1 microliter) caused an increase in slow wave sleep [36].

References