Utilizing immunohistochemistry for the c- fosprotein to detect neuronal activity, we examined the effects of continuous intravenous and intracerebroventricular infusion of interleukin (IL)-1βin the rat brain, and the involvement of prostaglandins (PGs) in IL-1β-induced c- fosexpression. Continuous intravenous infusion of IL-1β(10 ng/min) markedly augmented c- fosexpression in the paraventricular (PVN) and the supraoptic (SON) nuclei of the hypothalamus as well as in the central amygdaloid nucleus (CeA). The number of IL-1β-induced c- fos-positive cells in the PVN and SON was significantly lower in rats pretreated with indomethacin than in vehicle-treated rats. However, the number of IL1β-induced c- fos-positive cells in the CeA remained unchanged. c- fosprotein was induced after intracerebroventricular infusion of IL-1β(200 ng) in the PVN, SON and arcuate nuclei of the hypothalamus, and in the CeA. The induction of c- fosimmunoreactivity by central administration of IL-1βwas blocked by indomethacin (500µg/rat), except in the CeA. These findings suggest that PGs are involved in the complex transmission of signals from circulating or central IL-1βto hypothalamic neurons.