Abstract
It is now known that after an immobilization stress (IS) of short duration (1 h), adult rats exhibit a significant rapid eye movement (REM) sleep rebound. In this study, we examined this phenomenon in aged animals. We found that aged rats subjected to an IS did not show a sleep rebound after the restraint, in contrast to younger animals. Plasma corticosterone and corticotrophin (ACTH 1 – 39) levels were, however, similar in aged and adult rats. The corticotrophin-like intermediate lobe peptide (CLIP or ACTH 18 – 39) system of the arcuate nucleus, suggested to be involved in REM sleep genesis by way of pontine projections (HP: the hypothalamo–pontine axis), was also not different between aged and young rats. The lack of REM sleep rebound observed in aged animals is thus independent of the HPA (hypothalamo–pituitary–adrenal) and HP axe activities. The causal impairments might reside in REM sleep executive structures of the dorsal pontine tegmentum.
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