RT Book, Section A1 Nestler, Eric J. A1 Hyman, Steven E. A1 Holtzman, David M. A1 Malenka, Robert C. SR Print(0) ID 1105916372 T1 Sleep and Arousal T2 Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 3e YR 2015 FD 2015 PB McGraw-Hill Education PP New York, NY SN 9780071827690 LK neurology.mhmedical.com/content.aspx?aid=1105916372 RD 2024/11/07 AB Both sleep and arousal are active processes mediated by specific brain regions and neurotransmitter systems.Sleep can be divided into two phases, nonrapid eye movement (non-REM) and REM sleep, the latter being characterized by brain activity resembling that observed during the waking state.The different physiologic functions of sleep are unknown; a role in memory consolidation is likely.The initiation of non-REM sleep is controlled in part by GABAergic neurons in the preoptic/anterior hypothalamic area; the initiation of REM sleep is controlled by cholinergic cells in the pontine tegmentum.Sleep is controlled both by circadian rhythms and by the homeostatic drive produced by periods of wakefulness. Adenosine is an important mediator of the homeostatic drive for sleep.The suprachiasmatic nucleus is the primary pacemaker for the circadian regulation of sleep and other physiologic processes, in particular, for entraining circadian rhythms to environmental light.Circadian rhythms are produced, in part, by the complex transcriptional regulation of “clock” genes that have been conserved throughout evolution.Sleep disorders are a significant cause of morbidity. A major advance is the finding that decreased expression of the hypothalamic neuropeptide orexin (also called hypocretin) causes most human narcolepsy.Benzodiazepines and similarly acting drugs, which are positive allosteric modulators of GABAA receptors, are the most common pharmacologic treatments for insomnia.General anesthetics, comprising diverse classes of compounds, induce a non-REM sleep-like state characterized by amnesia, analgesia, immobility, and hypnosis. Most general anesthetics act, at least in part, by facilitating inhibitory ion channels (including ligand-gated channels) or inhibiting excitatory ion channels.