抄録
Prolonged wakefulness or sleep deprivation induces fatigue effects, such as drowsiness and a decrease in learning and memory in humans. A person taking a nap after sleep deprivation shows deep sleep, i.e., non-rapid eye movement (non-REM) sleep, for recovery from fatigue. However, the mechanism involved in these responses remains unclear. Previously, we demonstrated that prostaglandin (PG) D2-induced non-REM sleep was mediated by DP receptor (DPR) in mice. Sleep deprivation by gentle handling in the light period increased the PGD2 content in the brain of wild-type (WT) mice and induced the rebound of both non-REM sleep and REM sleep in a sleep deprivation-time dependent manner. However, the gene-knockout (KO) mice for PGD synthase (PGDS) or DPR did not show any rebound of non-REM sleep after sleep deprivation, indicating PGD2 to be crucial for induction of the non-REM sleep rebound to recover from sleep deprivation stress. Furthermore, we investigated the effect of sleep deprivation on spatial learning and memory for 5 days, as assessed by the Morris water maze test with the hidden platform. When we performed 6 h sleep deprivation before swimming from Day 2 to Day 5, WT mice increased drowsiness day by day to be inactive during the sleep deprivation treatment, whereas PGDS KO mice remained active even on Day 5. The sleep deprivation suppressed the decline of the escape latency as a function of training days for WT mice, but not at all for the KO mice, indicating that sleep deprivation induced PGD2-mediated drowsiness and impaired spatial learning and memory. [Jpn J Physiol 55 Suppl:S19 (2005)]
