Female hares were given an i.v. injection of 5-mu-g luteinizing-hormone-releasing hormone (LHRH) between Days 7 and 19 (n = 21), 20 and 33 (n = 17) and 34 and 41 (n = 17) of pregnancy, and in the 3 days after parturition (n = 16). Whatever the stage of pregnancy, the LHRH injection induced a release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and an acute secretion of progesterone; these hormonal responses increased significantly during pregnancy, to reach values similar to those observed in nonpregnant, nonpseudopregnant females during the breeding season in the 3 days after parturition. However, the release of LH remained monophasic in pregnant and post-partum females, in contrast to the unmated females during the reproductive season, in which there was a biphasic profile. The proportion of ovulating females after LHRH treatment was approximately 60% at the beginning and end of pregnancy; and, after parturition, fell to 23% between Days 20 and 33. After Day 33, the pituitary response to LHRH was significantly higher in ovulating than in nonovulating females. At the beginning of pregnancy, 67% of females aborted after LHRH injection; after Day 20, the incidence of abortion decreased significantly and was 0% from Day 34. The amplitude and duration of progesterone secretion by the new corpora lutea resulting from ovulation after LHRH injection were similar to those of corpora lutea induced in nonpregnant females during the breeding season. These results show that, throughout pregnancy, despite high circulating progesterone concentrations, the pituitary and the ovary can respond to an LHRH injection by a release of LH and FSH, and by an ovulation. Before Day 34, the neural pathways between mating stimuli and induced ovulation are therefore blocked mainly at the hypothalamic level; from Day 34, the pituitary content of LH and FSH increases, and mating can be followed by an endogenous release of LHRH sufficient to induce a gonadotrophin surge and an ovulation. The mechanisms overriding the hypothalamic blockade of induced ovulation and allowing superfoetation remain to be determined.