The purpose of this study was to determine which specific structures within the medial preoptic-anterior hypothalamic area are necessary to maintain cyclic ovulation in the rat, and to define the deifcit(s) in the feedback regulation of gonadotropin secretion associated with lesions that result in anovulation. Large (approximately 1.1 mm dia.) or small (approximately 0.7 mm dia.) electrolytic lesions were placed in several loci within preoptic, anterior hyopthalamic and suprachiasmatic areas in regularly cycling adult female rats. Large lesions which included the suprachiasmatic nuclei (SCN) induced an anovulatory condition characterized by persistent vaginal cornification and polyfollicular ovaries (persistent estrus). Large or small lesions which included the medial preoptic nucleus (MPN), a small periventricular column of cells located immediately caudal to the organum vasculosum of the lamina terminalis (OVLT), also induced persistent estrus. Lesions placed elsewhere within the medial preoptic-anterior hypothalamic area never induced persistent estrus but were frequently associated with repeated periods of prolonged diestrus separated by brief periods of vaginal cornification. These prolonged diestrous intervals appeared to be related to spontaneous luteal activation following ovulation rather than impaired folliculogenesis. LH and FSH surges induced by sequential administration of estradiol benzoate and progesterone (P) were completely abolished only by lesions which included the MPN. Small lesions involving only the MPN and OVLT or the MPN and caudally adjacent loci in the suprachiasmatic region were as effective in this respect as larger lesions encompassing most of the preoptic-suprachiasmatic region from the diagonal band of Broca to the rostral pole of the SCN. On the other hand, P-induced gonadotropin surges were never completely blocked by SCN lesions, although the magnitude of the surge was highly variable and frequently attenuated compared to controls. It is concluded that both the MPN and SCN are required for the long-term maintenance of spontaneous cyclic ovulation in the rat. However, the characteristically dissimilar deficits in P-induced gonadotropin release associated with lesions of one or the other of these structures indicate that these nuclei may play different roles in the regulation of gonadotropin surges. It is suggested that neural elements indispensable for phasic gonadotropin release are located within and/or immediately adjacent to the MPN. The SCN may influence phasic gonadotropin release indirectly, by regulating circadian rhythms which govern the responsiveness of other neural elements to hormonal stimuli.