KISSPEPTIN AND GNIH CONTROL OF GNRH IN FEMALE MAMMALS

Since the discovery of kisspeptin and gonadotropin-inhibitory hormone (GnIH) our understanding of the vertebrate reproductive physiology has greatly increased. Gonadotropin-releasing hormones (GnRH) is a hypothalamic decapeptide secreted into the hypothalamo-hypophyseal portal system in the median eminence. Pulsatile secretion of GnRH is prerequisite to secretion of gonadotropins (FSH and LH) from the gonadotropes in the pars distalis of the adenohypophysis, which control gonadal function in both males and females. Control of secretion of gonadotropins occurs vial the feedback actions of the gonadal hormones. Estradiol, depending on its blood concentration, may exert either a negative or positive feedback on gonadotropin (Gn) secretion, partly through its action of GnRH neurons and partly on the pituitary gland. A low level of estradiol decreases Gn secretion; however, in most mammals, estradiol secretion during the follicular phase of the ovarian cycle reaches to a peak level, which causes a sudden surge of gonadotropin secretion by exerting a positive feedback effect on the hypothalamus. In mammals, progesterone exerts a negative effect on Gn secretion. Because GnRH neurons do not express receptors for estradiol (ERα), androgens, and progesterone (PR), these hormones may affect the GnRH neurons through acting on various interneurons, known to be associated with the GnRH neurons. The axonal terminals of many interneurons are in close contact, and some of them also form synapses with the GnRH neurons.