The present study examines the function of several cytologically distinct suprachiasmatic structures in the regulation of ovulation and positive feedback effects of estrogen and progesterone on gonadotropin release in the rat. Small (0.6–0.8 mm dia.) electrolytic lesions were placed at four loci along the rostrocaudal extent of the suprachiasmatic region in regularly cycling female rats. Anovulatory persistent estrus occurred only when lesions were located either in the suprachiasmatic nucleus (SCN) or the medial preoptic nucleus (MPN), a small periventricular cell group lying immediately caudal to the organum vasculosum lamina terminalis (OVLT). Lesions restricted to the OVLT and adjacent ventral prechiasmatic region (VPC-L), or the anterior suprachiasmatic region (ASR) between the MPN and SCN resulted in irregular estrous cycles frequently marked by periods of prolonged diestrus. Following administration of 50 µg estradiol benzoate (EB) a daily afternoon surge of gonadotropin was observed in control animals. This circadian release of gonadotropins was completely abolished by SCN, ASR and MPN lesions. EB-induced gonadotropin surges were also greatly attenuated by VPC-L lesions. Subsequent administration of 1.5 mg progesterone (P) induced large surges of luteinizing hormone and follicle-stimulating hormone in VPC-L and ASR lesioned animals as well as controls. P administration also elicited gonadotropin surges in SCN lesioned animals, although surges were markedly attenuated in magnitude compared to controls. Only lesions that destroyed the MPN and immediately adjacent periventricular tissue completely and invariably eliminated P-induced gonadotropin release. Thus, anovulatory persistent estrus appears to be associated specifically with lesions that interfere with the positive feedback effect of P (MPN and SCN lesions). Animals with lesions that block or attenuate EB effects without interfering with P sensitive neural substrates can maintain long-term spontaneous ovulation (VPC-L and ASR lesions). An hypothesis is advanced to account for the differential effect of MPN and SCN lesions on P-induced gonadotropin release.