Two experiments were performed to test the importance of both pituitary and neural sites of action of estradiol in inducing the surge of luteinizing hormone (LH) in the ewe. Both experiments were conducted using an animal model in which pulsatile secretion of gonadotropin-releasing hormone (GnRH) and endogenous secretion of ovarian steroids were eliminated by ovariectomy during seasonal anestrus and treatment with Silastic implants which maintained a luteal-phase level of serum progesterone. The hormonal requirements for the surge were then evaluated by systematic application of GnRH and estradiol signals using pulsatile infusion pumps (for GnRH) and Silastic implants (for estradiol). In experiment 1 the circulating level of estradiol and frequency of GnRH pulses were increased either abruptly or progressively (i.e. mimicking the changes in the estrous cycle between luteolysis and just before the LH surge). Abrupt increments led to an LH surge in all ewes; progressive rises to the same absolute levels did not. However, sudden application of a further large increase in GnRH upon the progressive rise elicited an LH surge in every instance. In experiment 2, a GnRH pulse pattern known to be effective in inducing the LH surge was applied under conditions of differing estradiol concentration: no estradiol, basal estradiol, basal rising to peak estradiol. The GnRH signal elicited high-amplitude surges of LH only in the presence of a peak estradiol concentration. Our findings are consistent with the conclusion that two actions are required for a rise in estradiol to elicit a full-amplitude surge of LH in the ewe: an action on the brain to evoke a sudden increase in GnRH release and an action on the pituitary to maximize its response to GnRH.