title: Neurophysiology of sleep and wakefulness.
abstract: Wakefulness, NREM sleep, and REM sleep are three distinct states of existence. Each state has characteristic behavioral and physiologic patterns,and each has specific neurophysiologic mechanisms associated with its generation and control. Structures in the brainstem use various neurotransmitters to influence higher brain structures in the midbrain and cortex. The ARAS provides cholinergic, noradrenergic, and glutaminergic stimulation to the thalamus, hypothalamus, and basal forebrain resulting in cholinergic and glutaminergic excitation of the cortex. An active cortex that exhibits a characteristic pattern of desynchronized EEG manifests wakefulness. Various factors affect the need and timing of sleep onset. These factors influence the nucleus tractus solitarius, causing its noradrenergic projections to midbrain and forebrain structures to inhibit activity in the ARAS, resulting inactivation of inhibitory GABAergic thalamocortical projections to the cor-tex. During a state of decreased activation, the cortex exhibits a pattern of synchronized EEG. Transition between NREM sleep and REM sleep is controlled by noradrenergic neurons in the loci coeruleus and serotoninergic neurons in the raphe called REM-off cells and cholinergic neurons in the nucleus reticularis pontis oralis called REM-on cells. Other brain structures are involved in generation and control of REM sleep-related phenomena, such as eye movement and muscle atonia. During wakefulness, there is increased sympathetic tone and decreased parasympathetic tone that maintains most organ systems in a state of action or readiness. During NREM sleep, there is decreased sympathetic tone and increased parasympathetic activity that creates a state of reduced activity. REM sleep is characterized by increased parasympathetic activity and variable sympathetic activity associated with increased activation of certain brain functions. The states of wakefulness and sleep are characterized as stages that are defined by stereotypical EEG, EMG, and EOG patterns. Wakefulness stage has an EEG pattern predominated by the alpha rhythm. With onset of stage 1 sleep, the alpha rhythm attenuates, and an EEG pattern of relatively low voltage and mixed frequency is seen. Progression to stage 2 sleep is defined by the appearance of sleep spindles or K-complexes. Further progression into the deepest sleep stages 3 and 4 is defined by the occurrence of high-amplitude, low-frequency EEG activity. The progression of sleep stages occurs in cycles of 60 to 120 minutes throughout the sleep period. Various circadian environmental and ontologic factors affect the pattern of sleep stage occurrence.
authors.affiliation: Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. harris.cameron@mayo.edu
authors.forename: Cameron D
authors.initials: CD
authors.lastname: Harris
mesh_terms: D001679:Biogenic Amines / Q000378:metabolism; D004569:Electroencephalography; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D012894:Sleep Stages / Q000502:physiology*; D014851:Wakefulness / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D001679:Biogenic Amines; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid