engleski

Physiological Basis of Sleep / Regulation of sleep and wakefulness

Wakefulness is characterized by low-amplitude beta waves and alpha rhythm on the human EEG, whereas sleep is characterized by theta waves and spindles, as well as high-amplitude slow delta waves. There are two distinct states of sleep de
ned on the basis of several physiological parameters, rapid eye movement (REM) and non-REM (NREM). Extensive brain neuronal networks, composed of wakefulness-, NREM- and REM-promoting neurones, are involved in the regulation of wake–sleep and NREM–REM transitions. The wake- and sleep-promoting neurones appear to be mutually inhibitory. This mutually antagonistic relationship can give rise to behaviour similar to that seen with a ‘ip-op’ switch. The sleep–wake cycle is regulated by two separate biological mechanisms, which interact together and balance each other. This model is often referred to as the ‘twoprocess model’ of sleep–wake regulation, composed of Process C, that reects the ‘circadian rhythm’, and Process S, that reects the ‘sleep–wake homeostasis’. Sleep exerts a modulatory effect on levels of some hormones, whereas the biological timing system has a more pronounced effect on other hormones. Extensive lines of evidence indicate that melatonin plays an important role in the regulation of human sleep. The suprachiasmatic nucleus was identi
ed as a site of chronobiological effect of melatonin in terms of affecting phase-shifting, as well as induction of sleep. Sleep regulatory and thermoregulatory systems are inter-related. The sleep–wake cycle is coupled tightly to the circadian time–course of the core body temperature, but the homeostatic increase in sleep pressure does not inuence the thermoregulatory system. In this chapter, we summarize the homeostatic, circadian, genetic, hormonal and thermoregulation of the sleep–wake cycle.

sleep, wakefulness

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