Slow wave sleep

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. 

Rapid eye movement sleep. Sleep stage characterized by rapid movements of the eyes and asynchronous EEG activity in the theta-frequency (5-10Hz) range. Counterpart is slow wave sleep, characterized by other electrophysiological (synchronized low frequency l-2Hz, large amplitude EEG and neuronal sharp wave-ripple oscillations) and endocrine (growth hormone surge) activities. 

Slow waves (EEG delta activity) comprise 20%-50% of the epoch sleep spindles usually are present None Decreased from wake... 

Generic term usually applied to the deeper stages of NREM sleep (stages 3 and 4), so called because of the high proportion of slow wave activity (SWA). 

The synchronised oscillatory activity between the intrinsically linked thalamus and cortex. Under normal circumstances there is a level of activity which changes during the sleep-wake cycle increasing during periods of slow wave sleep. Excess synchrony occurs in conditions such as epilepsy. Thiazolidinedione... 

Godschalk M, Dzoljic M, Bonta I Slow wave sleep and a state resembling absence epilepsy induced in the rat by gamma-hydroxybutyrate. Eur J Pharmacol 44 103-111, 1977... 

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. 

As we relax in preparation for and pass into sleep, the active desynchronised awake EEG characterised by the low-amplitude (5-10 pV) high-frequency (10-30 Hz) beta waves becomes progressively more synchronised giving larger (20-30 pV) and slower (8-12 Hz) alpha waves, and then even slower (1-4 Hz) and bigger (30-150 pV) delta waves. This so-called slow-wave sleep is interrupted at intervals of some 1-2h by the break-up and desynchronisation of the EEG into an awake-like pattern. Since this is accompanied by rapid eye movements, even though sleep persists and can be deeper, the phase is known as rapid eye movement, REM or paradoxical, sleep. It is a time when dreaming occurs and when memory may be secured. 

Figure 22.4 Idealised EEG-like patterns in sleep and waking. When we are awake and aroused the EEG is desynchronised (a). As we become drowsy and pass into sleep the EEG waves become more synchronised with 8-12 Hz alpha waves (b), sleep spindles then appear (c) before the EEG becomes even more synchronised with slow (about 1-2 Hz) high-voltage waves characteristic of deep slow-wave sleep (SWS). About every 90 min this pattern is disrupted and the EEG becomes more like that in arousal (d) except that the subject remains asleep. This phase of sleep is also characterised by rolling, rapid eye movements, the so-called REM sleep. SWS is consequently also known as non-REM sleep. These tracings have been drawn to show the main features of the different EEG phases of sleep and as such are much simpler than those that are actually recorded...

The functions of these different phases of sleep are not at all clear but chronic sleep deprivation does eventually lead to death. It seems to be the slow-wave component of sleep (SWS) that is vital and it is thought to serve a restorative purpose. This would be consistent with its greater occurrence during the early stages of the sleep cycle when hormone secretion supports anabolic metabolism. If subjects are wakened every time they enter a period of REM sleep (evidenced by the EEG) there appears to be no overt harmful effect on their behaviour. In fact, REM sleep deprivation has even been used, with some claims of success, as a treatment for minor depression. However, there is an unproven belief that REM sleep is important for memory consolidation. 

Figure 22.5 Pathways involved in cortico-thalamic synchrony and EEG arousal. The ascending reticular activating system (ARAS) extends from the cephalic medulla through the pons and midbrain to the thalamus (see Moruzzi and Mayoun 1949). It is activated by impulses in collaterals of the spinothalamic sensory pathway running to specific thalamic nuclei (SpThNc) and in turn activates much of the cortex, partly through the non-specific thalamic nuclei (NspThNc), which also receive inputs from SpThNc and also via the nucleus basalis (NcB). Its stimulation is followed by EEG arousal. It is probable that reciprocal links between cortical areas and the thalamus, particularly NspThN, lead to slow-wave (8 Hz) cortical EEG synchrony and, in the absence of appropriate sensory input and ARAS activity, a sleep state...

Augment, or more probably, break up thalamic-cortico synchrony and its tendency to promote slow-wave EEG activity and non-REM sleep. Whether this results in full arousal, or merely a temporary disruption of sleep to give REM periods without full awaking, will depend on the balance of inputs and the overall state of cortical activity. 

Figure 22.9 Summary of the influence of varying factors on sleep and waking. The EEG is shown diagramatically in the typical arousal (awake) state and in both non-REM (slow wave) and REM sleep. Appropriate activity levels, high or low, are shown for the different factors such as light input, melatonin secretion or ACh, NA, and 5-HT function in the different phases...

BP 2.94) or (5) (Sch 50971) induce significant increases of slow-wave sleep or induce sedation in animal models [10, 33]. Potent and selective brain-penetrating H3 agonists could provide a new therapeutic option for the treatment of insomnia. 

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