[en] GnRH is the key neuropeptide controlling reproductive function in all vertebrate species. Two different neuroendocrine mechanisms have evolved among female mammals to regulate the mediobasal hypothalamic (MBH) release of GnRH leading to the preovulatory secretion of LH by the anterior pituitary gland. In females of spontaneously ovulating species, including rats, mice, guinea pigs, sheep, monkeys, and women, ovarian steroids secreted by maturing ovarian follicles induce a pulsatile pattern of GnRH release in the median eminence that, in turn, stimulates a preovulatory LH surge. In females of induced ovulating species, including rabbits, ferrets, cats, and camels, the preovulatory release of GnRH, and the resultant preovulatory LH surge, is induced by the receipt of genital somatosensory stimuli during mating. Induced ovulators generally do not show "spontaneous" steroid-induced LH surges during their reproductive cycles, suggesting that the positive feedback actions of steroid hormones on GnRH release are reduced or absent in these species. By contrast, mating-induced preovulatory surges occasionally occur in some spontaneously ovulating species. Most research in the field of GnRH neurobiology has been performed using spontaneous ovulators including rat, guinea pig, sheep, and rhesus monkey. This review summarizes the literature concerning the neuroendocrine mechanisms controlling GnRH biosynthesis and release in females of several induced ovulating species, and whenever possible it contrasts the results with those obtained for spontaneously ovulating species. It also considers the adaptive, evolutionary benefits and disadvantages of each type of ovulatory control mechanism. In females of induced ovulating species estradiol acts in the brain to induce aspects of proceptive and receptive sexual behavior. The primary mechanism involved in the preovulatory release of GnRH among induced ovulators involves the activation of midbrain and brainstem noradrenergic neurons in response to genital-somatosensory signals generated by receipt of an intromission from a male during mating. These noradrenergic neurons project to the MBH and, when activated, promote the release of GnRH from nerve terminals in the median eminence. In contrast to spontaneous ovulators, there is little evidence that endogenous opioid peptides normally inhibit MBH GnRH release among induced ovulators. Instead, the neural signals that induce a preovulatory LH surge in these species seem to be primarily excitatory. A complete understanding of the neuroendocrine control of ovulation will only be achieved in the future by comparative studies of several animal model systems in which mating-induced as well as spontaneous, hormonally stimulated activation of GnRH neurons drives the preovulatory LH surge.