Previously, we reported the involvement of brain ω-6 prostanoids, especially prostaglandin E2 and thromboxane A2, in the activation of central sympatho-adrenomedullary outflow in rats. ω-3 Prostanoids, including prostaglandin E3 and thromboxane A3, are believed to be less bioactive than ω-6 prostanoids, although studies on the functions of ω-3 prostanoids in the central nervous system have not been reported. In the present study, therefore, we compared the effects of centrally administered ω-3 prostanoids, prostaglandin E3 and thromboxane A3, with those of ω-6 prostanoids, prostaglandin E2 and thromboxane A2, on the plasma catecholamines in anesthetized rats. Intracerebroventricularly (i.c.v.) administered prostaglandin E2 (0.15, 0.3 and 1.5 nmol/animal) and prostaglandin E3 (0.3 and 3 nmol/animal) predominantly elevated plasma noradrenaline but not adrenaline, but the latter was less efficient than the former. On the other hand, U-46619 (an analog of thromboxane A2) (30, 100 and 300 nmol/animal, i.c.v.) and Δ17-U-46619 (an analog of thromboxane A3) (100 and 300 nmol/animal, i.c.v.) both elevated plasma catecholamines (adrenaline ≫ noradrenaline) to the same degree. These results suggest that centrally administered prostaglandin E3 is less effective than prostaglandin E2 to elevate plasma noradrenaline, and that thromboxane A3 is almost as equipotent as thromboxane A2 to elevate plasma catecholamines in rats.