Neuroanatomical and Neurochemical Bases of Vigilance States

Abstract

In the present chapter, hypotheses on the mechanisms responsible for the genesis of the three vigilance states, namely, waking, non-rapid eye movement (non-REM) also called slow-wave sleep (SWS), and REM sleep also called paradoxical sleep (PS), are presented. A huge number of studies first indicate that waking is induced by the activation of multiple waking systems, including the serotonergic, noradrenergic, cholinergic, and hypocretin systems. At the onset of sleep, the SWS-active neurons would be activated by the circadian clock localized in the suprachiasmatic nucleus and a hypnogenic factor, adenosine, which progressively accumulates in the brain during waking. A number of studies support the hypothesis that SWS results from the activation of GABAergic neurons localized in the ventrolateral preoptic nucleus (VLPO). However, new GABAergic systems recently described localized in the parafacial, accumbens, and reticular thalamic nuclei will be also presented. In addition, we will show that a large body of data strongly suggests that the switch from SWS to PS is due to the interaction of multiple populations of glutamatergic and GABAergic neurons localized in the posterior hypothalamus and the brainstem.

Keywords: Acetylcholine; Adenosine; Brainstem; GABA; Glycine; Histamine; Hypocretin; Melanin-concentrating hormone; Muscle atonia; Norepinephrine; Orexin; Serotonin.