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

Previous studies of total sleep deprivation (TSD) in the rat have show n an elevation of waking body temperature (T(b)) early in the deprivat ion period. TSD rats defend this rise behaviorally by selecting warm a mbient temperatures and autonomically by increasing heat production, t hus indicating an elevation of thermoregulatory setpoint. Prostaglandi ns (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 TS D and 13 control (TSC) rats in baseline and deprivation. During baseli ne. 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 admini stered on deprivation day 4. It produced a fall in waking T(b) in TSD rats from its deprivation-induced elevation. The difference between th e response to aspirin during baseline and during deprivation was signi ficant (-0.25-degrees-C. p < 0.05) for TSD rats but not TSC rats ( 0.1 7-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 P GD2 promotes lower T(b) and sleep in rats but PGE2 has opposite effect s, the results are consistent with a shift from PGD2 predominance in b aseline toward PGE2 predominance during TSD. However, the increase in sleepiness that occurs with sleep deprivation is more consistent with a shift toward PGD2 predominance.