The neurophysiology and neurobiology of wakefulness and non-rapid eye movement (NREM) sleep

International audienceWaking results from the activity of multiple neurotransmitter/modulatory systems distributed throughout the brain. According to the current model, both circadian signals and the progressive accumulation of hypnogenic factors (e.g., adenosine) during prolonged period of wakefulness ultimately activate non-rapid eye movement- promoting neurones. A number of convincing studies support the hypothesis that non-rapid eye movement sleep results from the activation of gamma-aminobutyric acid ergic neurones localized at least in the preoptic area of the anterior hypothala- mus leading to the inhibition of the wake-active neurones widely distributed within the whole brain. However, recent studies identified a collection of additional neu- ronal (sub-)populations, whose activity correlates with, and facilitates, either wake- fulness or non-rapid eye movement sleep. The present chapter summarizes current hypotheses on the mechanisms underlying the onset, maintenance, and termination of waking and non-rapid eye movement sleep, also called slow-wave sleep