Role of corticosterone on sleep homeostasis induced by REM sleep deprivation in rats

• Published in: PloS one Vol. 8; no. 5; p. e63520
• Main Authors: Machado, Ricardo Borges, Tufik, Sergio, Suchecki, Deborah
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 07-05-2013; Public Library of Science (PLoS)
• Subjects: Adrenocorticotropic hormone; Animals; Biology; Brain research; Corticosterone; Corticosterone - administration & dosage; Corticosterone - pharmacology; Corticotropin; Electrodes; Eye movements; Gene expression; Glucocorticoids; Homeostasis; Homeostasis - drug effects; Hormones; Hypoglycemia; Hypothalamo-Hypophyseal System - drug effects; Hypothalamo-Hypophyseal System - physiopathology; Male; Metabolism; Metyrapone - administration & dosage; Metyrapone - pharmacology; NREM sleep; Physiological aspects; Pituitary-Adrenal System - drug effects; Pituitary-Adrenal System - physiopathology; Plasma levels; Psychobiology; Rapid eye movement state; Rats; Rats, Wistar; Recovery; REM sleep; Rodents; Sleep; Sleep (REM); Sleep deprivation; Sleep Deprivation - physiopathology; Sleep, REM - drug effects; Steroids (Organic compounds); Stress; Time Factors; Wakefulness - drug effects; Wakefulness - physiology; Brazil
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0063520

Sleep is regulated by humoral and homeostatic processes. If on one hand chronic elevation of stress hormones impair sleep, on the other hand, rapid eye movement (REM) sleep deprivation induces elevation of glucocorticoids and time of REM sleep during the recovery period. In the present study we sought to examine whether manipulations of corticosterone levels during REM sleep deprivation would alter the subsequent sleep rebound. Adult male Wistar rats were fit with electrodes for sleep monitoring and submitted to four days of REM sleep deprivation under repeated corticosterone or metyrapone (an inhibitor of corticosterone synthesis) administration. Sleep parameters were continuously recorded throughout the sleep deprivation period and during 3 days of sleep recovery. Plasma levels of adrenocorticotropic hormone and corticosterone were also evaluated. Metyrapone treatment prevented the elevation of corticosterone plasma levels induced by REM sleep deprivation, whereas corticosterone administration to REM sleep-deprived rats resulted in lower corticosterone levels than in non-sleep deprived rats. Nonetheless, both corticosterone and metyrapone administration led to several alterations on sleep homeostasis, including reductions in the amount of non-REM and REM sleep during the recovery period, although corticosterone increased delta activity (1.0-4.0 Hz) during REM sleep deprivation. Metyrapone treatment of REM sleep-deprived rats reduced the number of REM sleep episodes. In conclusion, reduction of corticosterone levels during REM sleep deprivation resulted in impairment of sleep rebound, suggesting that physiological elevation of corticosterone levels resulting from REM sleep deprivation is necessary for plentiful recovery of sleep after this stressful event.