SLEEP-DEPRIVATION IN THE RAT .17. EFFECT OF ASPIRIN ON ELEVATED BODY-TEMPERATURE

Previous studies of total sleep deprivation (TSD) in the rat have shown an elevation of waking body temperature (T(b)) early in the deprivation period. TSD rats defend this rise behaviorally by selecting warm ambient temperatures and autonomically by increasing heat production, thus indicating an elevation of thermoregulatory setpoint. Prostaglandins (PGs) can elevate setpoint and T(b). To investigate whether the TSD-induced rise in setpoint and T(b) was mediated by PGs, aspirin. which blocks the synthesis of PGs, was administered 100 mg/kg s.q. to 11 TSD and 13 control (TSC) rats in baseline and deprivation. During baseline. aspirin produced a nonsignificant (0.16-degrees-C) rise across all rats in waking T(b). For the sampled time period, waking T(b) during deprivation day 3 was significantly elevated in TSD rats (0.64-degrees-C, p < 0.01) but not in TSC rats (0.27-degrees-C). Aspirin was administered on deprivation day 4. It produced a fall in waking T(b) in TSD rats from its deprivation-induced elevation. The difference between the response to aspirin during baseline and during deprivation was significant (-0.25-degrees-C. p < 0.05) for TSD rats but not TSC rats ( 0.17-degrees-C). Time awake after aspirin increased significantly (16.2%, p < 0.05) during baseline and declined nonsignificantly (1.1%) during deprivation. These data imply that at least part of the rise in T(b) that is characteristic of TSD is mediated by PGs. To the extent that PGD2 promotes lower T(b) and sleep in rats but PGE2 has opposite effects, the results are consistent with a shift from PGD2 predominance in baseline toward PGE2 predominance during TSD. However, the increase in sleepiness that occurs with sleep deprivation is more consistent with a shift toward PGD2 predominance.