Slow wave activity

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). 

Some evidence supports a hypothesis that the POA hypnogenic system also plays a role in homeostatic control of sleep. Homeostatic control of NREM sleep refers to compensatory increases in sleep amounts and particularly in EEG slow wave activity (SWA, usually 0.5-4 Hz) after sleep deprivation. SWA is the hallmark of homeostatic control. SWA gradually declines within sustained sleep, as homeostatic drive for sleep is satisfied. A role for the POA in homeostasis is suggested by the following observations. 

Meerlo, P., de Bruin, E. A., Strijkstra, A. M. Daan, S. (2001). A social conflict increases EEG slow-wave activity during subsequent sleep. Physiol. Behav. 73, 331-5. 

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... 

This belief was further supported by the evidence of a correlation between the clinical response and REM sleep suppression as well as a temporal relationship between the onset of clinical response and REM sleep suppression. However, some of the later studies suggested that REM sleep suppression is not necessary for the antidepressant action (Gillin 1983). For example, some studies show evidence of no change or even an increase in REM sleep with the treatment of depression (Gillin et al. 2001). Recently, Landolt Gillin (Landolt and Gillin 2002) have also demonstrated that the antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of slow wave activity in non-REM sleep. However, the generalization of some of these studies is limited because of their small sample size. 

The importance of adenosine deaminase in the duration and intensity of sleep in humans has been noted recently (Retey et al. 2005). Animal studies suggest that sleep needs are genetically controlled, and this also seems to apply in humans. Probably, a genetic variant of adenosine deaminase, which is associated with the reduced metabolism of adenosine to inosine, specifically enhances deep sleep and slow wave activity during sleep. Thus low activity of the catabolic enzyme for adenosine results in elevated adenosine, and deep sleep. In contrast, insomnia patients could have a distinct polymorphism of more active adenosine deaminase resulting in less adenosine accumulation, insomnia, and a low threshold for anxiety. This could also explain interindividual differences in anxiety symptoms after caffeine intake in healthy volunteers. This could affect the EEG during sleep and wakefulness in a non-state-specific manner. 

Electrophysiological Tobacco smoking produces cortical activation on the EEG. Broadly, it reduces slow-wave activity (theta and delta) and increases activity in alpha and beta frequency bands (Knott et al. 1998 Pritchard et al. 1999). Other studies have found more isolated effects in alpha frequencies (Domino and Matsuoka 1994 Foulds et al. 1994). 

Intraperitoneal injections of eugenol and its natural analogs produce unconsciousness in rats, accompanied by slow-wave activity on the EEC (Sell and Carlini 1976). Cerebral levels of dopamine, norepinephrine, and serotonin are not apparently altered. 

The EEG will often show diffuse slow-wave activity in the 5 to 7 cps range. The more severe episodes usually occur in patients who accidentally or purposely overdose on lithium, and this may lead to other medical complications, such as pulmonary edema, pneumonia, and cardiac arrhythmias. 

Franken P, Tobler I, Borbely AA. Sleep homeostasis in the rat simulation of the time course of EEG slow-wave activity [published erratum appears in Neurosci Lett 1991 Nov 11 132(2) 279]. Neurosci Lett 1991 130 141-144. 

Enhancements in NREM sleep (increases in NREM sleep time and intensity) as assessed by EEG slow-wave activity occur in response to GHRH admin-... 

Intracerebral or systemic administration of IL-1 P enhances NREM sleep in mice, rats, rabbits, cats, monkeys, and humans (reviewed in Refs. 40,46), and TNF-a promotes NREM sleep in rabbits, mice, rats, and sheep (reviewed in Refs. 40,46). Both NREM sleep time and intensity (EEG slow-wave activity) increase after IL-1 3 or TNF-a. In rats and cats, only low doses of IL-1 stimulate NREM sleep. In contrast, higher doses decrease NREM sleep, perhaps owing to IL-ip-induced stimulation of corticotropin-releasing hormone (CRH), which is known to suppress NREM sleep (55,56). A correlation is observed between plasma TNF-a concentrations and sleepiness or fatigue in a number of clinical conditions. Thus, TNF-a is... 

Hypothalamic content and mRNA levels of TNF-a peak during the early light period, when NREM sleep is maximal, in the rat (70,71). IL-1-like activity varies with the sleep-wake cycle in the cerebrospinal fluid of cats (72). IL-lp protein levels in plasma (73) and hypothalamic IL-lp mRNA levels (74) are highest during the sleep period in rats. Sleep deprivation increases IL-ip and TNF-a mRNA levels in the hypothalamus (75-77) and expression of the 55-kD TNFR is also stimulated in the brain (77). In humans, peak levels of IL-1 occur at sleep onset in the blood (78) and IL-1 blood levels also increase during sleep deprivation (79). Blood levels of TNF-a correlate with EEG slow-wave activity (80), and concentrations of circulating TNF-a and the soluble 55-kD TNFR increase after sleep deprivation in humans (81). 

Kaushal N, Johansson B, Halldner L, Fredholm B, Greene RW. Reduced slow wave activity in the adenosine Al receptor knockout mice. Soc Neurosci Abstr 2002 27 2378. 

Kapas L, Obal F, Jr., Alfoldi P, Rubicsek G, Penke B, Obal F. Effects of nocturnal intraperitoneal administration of cholecystokinin in rats simultaneous increase in sleep, increase in EEG slow-wave activity, reduction of motor activity, suppression of eating, and decrease in brain temperature. Brain Res 1988 438 155-164. 

Fig. 1. Time course of slow wave activity (SWA 0.5 1 Hz) during the first NREM period in 21 major depressed (MD) patients age and gender matched to 21 healthy volunteers (HV) (Period effects < 0.0001 group effects NS Period x Group < 0.05)...

Armitage R, Hoffmann RF, Trivedi M, Rush JA (2000) Slow wave activity in NREM sleep sex and age effects in depressed outpatients and healthy controls. Psychiatry Res 95 201-213... 

Quantitative EEG analysis has been used to investigate the effects of zolpidem on delta (slow wave) activity in poor sleepers and chronic insomniacs. Benoit et al. 

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