Homeostasis of REM Sleep After Total and Selective Sleep Deprivation in the Rat

Abstract

During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was approximately 1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

“…In parallel, further complicatedness in the understanding of sleep mechanism has been pointed-out due to that circadian and homeostatic factors influence sleep processes (Curie et al, 2013Houben et al, 2014;Borbely et al, 2016). In regard to the homeostatic clout in sleep modulation and consistent with previous reports, it is known that a compensatory enhancement in the intensity and duration of sleep known as ''sleep rebound" is present as a result of significative loss of sleep (Borbely and Achermann, 1999;Schwierin et al, 1999;Ocampo-Garces et al, 2000;Vyazovskiy et al, 2007Vyazovskiy et al, , 2011Borbely et al, 2016). Additionally, the total sleep deprivation (TSD) is accompanied with an accumulation of endogenous neurochemicals, including dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT), as well as adenosine (AD).…”

The effects of rapid eye movement sleep deprivation and recovery on spatial reference memory of young rats

“…It is well known that RSD could induce compensatory mechanisms and cause rebound of REM sleep during the recovery period (Machado et al, 2004;Ocampo-Garcés et al, 2000;. This phenomenon was considered to be a homeostatic compensation for a deficit in REM sleep (Ocampo-Garcés et al, 2000); however, the functional significance for memory is unclear.…”

“…This phenomenon was considered to be a homeostatic compensation for a deficit in REM sleep (Ocampo-Garcés et al, 2000); however, the functional significance for memory is unclear. There is electrophysiological evidence that REM rebound does not restore the RSD-induced impairment of LTP (Ishikawa et al, 2006;Kim et al, 2005;Romcy-Pereira & Pavlides, 2004).…”

“…l In developing an adaptation of the MMPM for young rats, we relied on behavioral observations during pilot studies in order to determine the optimal size of the platform. The platform size finally identified as ideal for REM sleep deprivation in this age rat was sufficiently small (4.0-cm diameter) to initially allow the youngest Garcés, Molina, Rodriguez, & Vivaldi, 2000;Suchecki, Duarte Palma, & Tufik, 2000). More recent research has further demonstrated that REM rebound happened in the first 24 h after 96 h of RSD (Machado, Hipólide, Benedito-Silva, & Tufik, 2004).…”

Activation of Phasic Pontine-Wave Generator Prevents Rapid Eye Movement Sleep Deprivation-Induced Learning Impairment in the Rat: A Mechanism for Sleep-Dependent Plasticity

“…(2) The moving disc or drum method (Stefurak et al, 1977;Rechtschaffen and Bergmann, 1995;Feng et al, 2000;Campbell et al, 2002): Although less stressful than the flowerpot method, this procedure significantly reduces the amount of SWS and introduces an unrelated variable physical activity. (3) Gentle handling (Vogel, 1975;Ocampo-Garces et al, 2000;Sei et al, 2000;Vyazovskiy et al, 2002): This method disrupts SWS in addition to REM sleep. To reduce some of the disadvantages encountered with the existing methods of REM sleep deprivation, we designed a new method that should minimize extraneous stress and physical activity and eliminate the need for the experimenter's physical proximity to the rat.…”