Brain inhibitory mechanisms involved in basic and higher integrated sleep processes

Abstract

Brain function is supported by central activating processes that are significant during waking, decrease during slow wave sleep following waking and increase again during paradoxical sleep during which brain activation is as high as, or higher than, during waking in nearly all structures. However, inhibitory mechanisms are crucial for sleep onset. They were first identified by behavioral, neuroanatomical and electrophysiological criteria, then by pharmacological and neurochemical ones. During slow wave sleep, they are supported by GABAergic mechanisms located at midbrain, mesopontine and pontine levels but are induced and sustained by forebrain and hindbrain influences. GABAergic processes are also responsible for paradoxical sleep occurrence, particularly by suppression of noradrenaline and serotonin (5-HT) inhibition of paradoxical sleep-generating structures. Hindbrain and forebrain modulate these structures situated at the mesopontine level. For sleep mentation, the noradrenergic and serotonergic silence is thought, today, to be directly, or indirectly, responsible for dopamine predominance and glutamate decrease in the nucleus accumbens, which could be the background of the well-known psychotic-like mental activity of dreaming.