Abstract
In the present chapter, we are providing state-of-the-art hypotheses on the mechanisms responsible for the succession of the three vigilance states: waking; non–rapid eye movement (non-REM, or NREM) sleep, also called slow-wave sleep (SWS); and REM sleep, also called paradoxical sleep (PS). It is proposed that waking is induced by the activity of multiple waking systems, including the serotonergic, noradrenergic, cholinergic, and hypocretin systems. In contrast, a number of studies indicate that the GABAergic neurons that induce SWS are all localized in the ventrolateral preoptic nucleus (VLPO) and surrounding structures. At the onset of sleep, the PS sleep neurons are activated by the circadian clock localized in the suprachiasmatic nucleus and a hypnogenic factor, adenosine, which progressively accumulates in the brain during waking. Finally, we review data strongly suggesting that the switch from SWS to PS sleep is due to the interaction of multiple populations of glutamatergic and GABAergic neurons localized in the hypothalamus and the brainstem.
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