Abstract
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.
Highlights
IntroductionStress hormones are of great importance, given the negative influence that certain forms of chronic stress have on sleep, both in humans [1,2,3] and animals [4,5,6,7]
Sleep homeostasis is regulated by humoral, circadian and homeostatic factors
REM sleep-deprivation (REMSD) rats treated with corticosterone displayed lower CORT levels than their respective CTL group (235.01%, p#0.0005), whereas no difference between these groups was seen with metyrapone
Summary
Stress hormones are of great importance, given the negative influence that certain forms of chronic stress have on sleep, both in humans [1,2,3] and animals [4,5,6,7]. It is manifested after long periods of forced awakening, after which a period of compensatory sleep ensues, with augmented NREM and REM sleep [21,22]. Long periods of total sleep deprivation may results either in no or negative (under basal levels) NREM sleep rebound (see [28] for review). Changes in sleep microarchitecture, involving both low and high frequencies bands, have been reported after total or partial sleep deprivation procedures, in humans [29,30,31] and animals [25,32,33,34]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
