Why do we sleep?

Abstract

According to a simple behavioral definition, sleep is a reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment. Sleep is dividing into two states: Non-rapid eye movement (NREM) sleep which is subdivided into three stages (N1, N2, N3); and rapid eye movement (REM) sleep characterized by rapid eye movements, muscle atonia and desynchronized EEG. Mammalian sleep and wake states are regulated by multiple neuronal systems located in the brainstem, diencephalon, and telencephalon. Wakefulness is maintained by activation of the ascending reticular activating system involving several neurotransmitters including glutamate, acetylcholine and the monoamines. NREM sleep onset is associated with a reduction in activation of the ascending reticular activating system and an increase in neural activity within the ventrolateral preoptic area, anterior hypothalamus and basal forebrain. REM sleep is triggered by activation of cholinergic neurons in the laterodorsal and pedunculopontine tegmental nuclei. The suppression of motor activity in REM sleep is generated by glutamate-mediated activation of descending medullary reticular formation. The two-process model postulates that a homeostatic process rises during waking and declines during sleep and interacts with a circadian process that is not directly dependent of sleep and waking. Sleep function remains controversial. Sleep is thought to be restorative, conservative, adaptive, thermoregulatory and memory consolidative functions. Sleep also serves host-defense mechanisms and conserves caloric expenditures. Emerging evidences indicated that sleep replenishes brain energy stores and that sleep serves a glymphatic function by removing toxic byproducts of waking activity. Finally, there is experimental evidence that connectivity changes with sleep, sleep loss, and with changing afferent input, and that those changes are linked to sleep regulatory mechanisms. Sleep medicine as a medical specialty has existed for more than 30 years. The study on over 90 kinds of sleep disorders has shed light on the understanding to the mechanisms of sleep. For example, the finding of the role of hypocretin/orexin in the patho-physiology of narcolepsy led to the reveal of hypocretin/orexin as a major wakefulness promoting substance. The evolution of the field will help us recognize the impact of sleep disorders on society as well as the nature of sleep itself.