Summary Prolonged rapid eye movement sleep deprivation (REMSD) causes hypothermia and death; however, the effect of deprivation within 24 h and its mechanism(s) of action were unknown. Based on existing reports we argued that REMSD should, at least initially, induce hyperthermia and the death upon prolonged deprivation could be due to persistent hypothermia. We proposed that noradrenaline (NA), which modulates body temperature and is increased upon REMSD, may be involved in REMSD- associated body temperature changes. Adult male Wistar rats were REM sleep deprived for 6–9 days by the classical flower pot method; suitable free moving, large platform and recovery controls were carried out. The rectal temperature (Trec) was recorded every minute for 1 h, or once daily, or before and after i.p. injection of prazosin, an alpha-1 adrenergic antagonist. The Trec was indeed elevated within 24 h of REMSD which decreased steadily, despite continuation of deprivation. Prazosin injection into the deprived rats reduced the Trec within 30 min, and the duration of effect was comparable to its pharmacological half life. The findings have been explained on the basis of REMSD-induced elevated NA level, which has opposite actions on the peripheral and the central nervous systems. We propose that REMSD-associated immediate increase in Trec is due to increased Na-K ATPase as well as metabolic activities and peripheral vasoconstriction. However, upon prolonged deprivation, probably the persistent effect of NA on the central thermoregulatory sites induced sustained hypothermia, which if remained uncontrolled, results in death. Thus, our findings suggest that peripheral prazosin injection in REMSD would not bring the body temperature to normal, rather might become counterproductive.