Influence of stress duration on the sleep rebound induced by immobilization in the rat: a possible role for corticosterone

Abstract

In rats, recovery from short intense stress usually involves a sleep rebound characterized by an increase in slow-wave sleep and paradoxical sleep duration. However, a large body of evidence indicates that stressful situations lasting for several days or weeks can have deleterious effects on sleep quantity and quality, probably leading to an impairment of the sleep rebound. In this study, using immobilization as a stress model in the rat, we sought to determine the stress duration beyond which the sleep rebound disappears, as well as the mechanisms responsible for this suppression. In a first series of experiments, rats were immobilized for 30 min, 1 h, 2 h or 4 h. Slow-wave sleep rebounds evidenced after the different immobilization periods were, respectively, +32%, +25%, +9% and −0.2% and paradoxical sleep rebounds +57%, +88%, +103% and +21% compared with control recordings of the same animals. The sleep rebound thus disappeared when the duration of immobilization reached 4 h. In a second series of experiments, adrenalectomized rats were subjected to a 1 h immobilization, and showed an increased slow-wave sleep rebound (+44% compared to intact ones), whereas the paradoxical sleep rebound was slightly decreased and delayed. When glucocorticoid action was replaced by an intramuscular injection of dexamethasone, a glucocorticoid receptor agonist, the sleep rebound was suppressed (−3% in slow-wave sleep and −37% in paradoxical sleep). Lastly, in a third series of experiments, plasma corticosterone concentration was evaluated at different times in rats immobilized for 1 h or 4 h. Corticosterone concentration was higher in stressed animals than in control ones (+92%) and returned to baseline 4 h earlier in animals immobilized for 1 h compared with those stressed for 4 h. Therefore, corticosterone is probably involved in the suppression of the sleep rebound after long immobilization periods since (i) dexamethasone suppressed the stress-induced sleep rebound, and (ii) corticosterone was elevated for a longer period in the 4 h immobilization group. It is concluded that the reparative sleep rebound is suppressed after long and intense stress periods and that a prolonged glucocorticoid secretion could be one of the factors responsible for this effect. This deleterious effect on sleep could impair normal recovery and quick adaptation to a new situation, and could participate in the development of stress-related pathologies in humans.