GABAergic system inducing hyperthermia in the rat preoptic area: its independence of prostaglandin E2 system.

Brain temperature of conscious freely moving rats was recorded during perfusion of the preoptic area (POA) with neuroactive compounds using the microdialysis technique. Unilateral perfusion of the POA with the sodium channel blocking agent, tetrodotoxin (1 microM), induced a pronounced hyperthermia. Of the neuroactive compounds examined, the greatest thermogenic response to local perfusion of the POA was elicited by the GABAergic agonist, muscimol. Muscimol (10, 20 and 100 microM) exhibited a dose-dependent and reversible hyperthermia. This hyperthermia was attenuated by co-perfusion with the GABAergic antagonist, bicuculline (10 microM). Muscimol-induced hyperthermia was independent of prostaglandin biosynthesis, and additive with prostaglandin E2 (10 microM)-induced hyperthermia. Prostaglandin E2-induced hyperthermia was not affected by co-perfusion with bicuculline. These data suggest the existence of two independent neurochemical systems for genesis of hyperthermia colocalized within the POA.