Slow wave sleep, effects

The class III cytokine receptor family includes two TNE receptors, the low affinity NGE receptor and 7-ceU surface recognition sites that appear to play a role in proliferation, apoptosis, and immunodeficiency. TNE-a (- 17, 000 protein) is produced by astrocytes and microglia and can induce fever, induce slow-wave sleep, reduce feeding, stimulate prostaglandin synthesis, stimulate corticotrophin-releasing factor and prolactin secretion, and reduce thyroid hormone secretion. TNE-a stimulates IL-1 release, is cytotoxic to oligodendrocytes, and reduces myelination this has been impHcated in multiple sclerosis and encephalomyelitis. Astrocyte TNE-a receptors mediate effects on IL-6 expression and augment astrocytic expression of MHC in response to other stimulants such as lEN-y. 

Scrima L, Hartman PG, Johnson EH, et al The effects of gamma-hydroxybutyrate on the sleep of narcolepsy patients a double blind study. Sleep 13 479 90, 1990 Series F, Series 1, Cormier Y Effects of enhancing slow-wave sleep by gamma-hydroxybutyrate on obstructive sleep apnea. Am Rev Respir Dis 143 1378-1383, 1992 Shannon M Methylenedioxymethamphetamine (MDMA, ecstasy ). Pediatr Emerg Care 16 377-380, 2000... 

An MRL of 0.1 ppm was derived for intermediate inhalation exposure (15-364 days) to trichloroethylene. This MRL was based on a study by Arito et al. (1994a) in which male JCL-Wistar rats were exposed to 0, 50, 100, or 300 ppm trichloroethylene for 6 weeks, 5 days/week, 8 hours/day. A LOAEL of 50 ppm was observed for decreased wakefulness during exposure, and decreased postexposure heart rate and slow wave sleep. Another study with rats found an increase in sleep-apneic episodes and cardiac arrhythmias after exposure to trichloroethylene (Arito et al. 1993). These results corroborate similar effects observed in humans exposed to trichloroethylene, as described in the previous paragraph, as well as evidence of organic solvent-induced sleep apnea in humans (Edling et al. 1993 Monstad et al. 1987, 1992 Wise et al. 1983). 

Effects noted in study and corresponding doses Decreased post-exposure heart rate and slow wave sleep were observed at 50 ppm (less serious LOAEL). Decreased wakefiilness was observed during the exposures. Disturbed heart rates and sleep patterns (sleep apnea) have been seen in human exposures to organic solvents as well. 

Figure 4.1 Effect of an iontophoretic injection of bicuculline, a GABAa antagonist, on a locus coeruleus noradrenergic neuron. With reduced activity during slow wave sleep, this neuron then becomes silent during paradoxical sleep (PS). The application of bicuculline reversibly restores tonic discharge, indicating the role of GABA in the cessation of activity of this neuron during PS.

Hoppenbrouwers, M. L. Van den Busche, G. (1987). Mioflazine, a nucleoside transport inhibitor effective as sleep promotor in humans . Abstract, International Symposium Current Trends in Slow Wave Sleep Research, Beerse, Belgium, p. 38. 

Intracerebroventricular infusion of CST-14 dramatically increases the amount of slow wave activity in rats, at the expense of wakefulness. The mechanism by which CST-14 enhances cortical synchronization has been established through the interaction of CST-14 with acetylcholine, a neurotransmitter known to be involved in the maintenance of cortical desynchronization. Application of acetylcholine (ACh) in the anesthetized animal increases fast activity, and this effect is blocked with the simultaneous addition of CST-14. These data suggest that CST-14 increases slow wave sleep by antagonizing the effects of ACh on cortical excitability. In addition to this mechanism, cortistatin may enhance cortical... 

BZD effects on human sleep are well characterized (Mendelson 2001) (a) decreased sleep latency (b) decreased awakenings (c) increased stage II sleep (d) suppressed stage III and IV sleep (e) increased REM sleep latency (f) initial reduction and fragmentation of REM sleep. Discontinuation of BZD treatment after three to four weeks produces a rebound of REM sleep as well as slow-wave sleep (SWS). BZD and non-BZD compounds are pharmacological agents indicated in the management of anxiety, insomnia, and other conditions in which anxiety is the main symptom, and should be considered as symptomatic medications (Nishino et al. 2004). 

Polysomnographic sleep research has demonstrated that besides disturbances of sleep continuity in depression, sleep disturbance is also characterized by a reduction of slow-wave sleep and a disinhibition of REM sleep, with a shortening of REM latency, a prolongation of the first REM period, and increased REM density [62]. Most effective antidepressant agents suppress REM sleep, and depressive symptoms are at least transiently alleviated by manipulations of the sleep-wake cycle, such as sleep deprivation or a phase advance of the sleep period [63]. Thus, there appears to be a bidirectional relationship between sleep, sleep alterations and mood. 

The EEG effects of valerian are most concordant with those of tiagabine, a GABA uptake inhibitor used to treat epilepsy. Tiagabine also increases slow-wave sleep, but unlike valerian has little or no effect on REM (Lancel et al. 1998). GABAA agonists also tend to have this effect. 

Vogel (186) reported that selective disruption of REM sleep, without interrupting slow-wave sleep, produced a gradual but sustained antidepressant effect. 

Typical complications include insomnia and excessive daytime sleepiness due to frequent nighttime awakenings. Sleep electroencephalogram (EEG) reveals absent or decreased slow-wave sleep, and, in some patients, early-onset REM sleep. If untreated, long-term effects of sleep apnea include increased incidence of hypertension vascular events (e.g., myocardial infarction, stroke) poor work performance increased risk of traffic accidents and stress in personal relationships ( 22, 23). 

The effects of acute systemic dexamethasone administration on sleep structure have been investigated. Dexamethasone caused significant increases in REM latency, the percentage time spent awake, and the percentage time spent in slow-wave sleep. There were also significant reductions in the percentage time spent in REM sleep and the number of REM periods (SEDA-21, 413 97). 

Ferrara M, De Gennaro F, Bertini M. The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening. Physiol Behav 1999 68 55-61. 

Benoit O, Foret J, Bouard G. The time course of slow wave sleep and REM sleep in habitual long and short sleepers effect of prior wakefulness. Hum Neurobiol 1983 2 91-96. 

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