To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E(2) (PGE(2)), PGE(2) and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (T-co) were observed in a 23 +/- 1 degrees C environment. 17-Phenyl-omega-trinor-PGE(2) (an EP(1) agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in T-co. Even though the EP(1) agonist was 10 times less potent than PGE(2) on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE(2)-induced one. No fever was elicited by an LCV injection of butaprost (an EP(2) agonist; 0.1-100 nmol), 11-deoxy-PGE(1) (an EP(2) agonist; 0.1-1.0 nmol), or MB-28767 (an EP(3) agonist; 0.01-1.0 nmol). The PGE(2) (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP(1) antagonist. The results suggest that the PGE(2)-induced hyperthermia in the rat is mediated predominantly through EP(1) receptors in the brain.