We previously reported that intraventricular prostaglandins (PGs) produced hyperthermia and hyperglycemia in anesthetized rats. However, the relationship of them is little known. We examined the relationship between hyperthermia and hyperglycemia induced by intraventricular PGF2α using curarized and adrenal demedullated rats. IV curare completely prevented the PGF2α-induced hyperthemia, but enhanced the hyperglycemic effect of PGF2α. Adrenal demedullation completely prevented the hyperglycemia, but did not affect the hyperthermic effect of PGF2α. To further assess the site of action concerned with PGF2α-induced thermoregulation and glucoregulation in the central nervous system (CNS), we injected saline or PGF2α into the preoptic area of the anterior hypothalamus (POA) in intact rats. After microinjection of PGF2α into the POA, the rectal temperature rose, but the plasma glucose level did not increase significantly, as compared with saline-treated control rats. These results suggest that PGF2α causes the central nervous system to produce hyperthermia via shivering, stimulated the somatic motor system, and to produce hyperglycemia by stimulating central sympathetic outflow to the adrenal medulla, but these operate independently under different neural regulation, and these sensitive sites are organically dissociated in the CNS.