Along-standing axiom in endocrine physiology is that normal reproductive function requires a highly coordinated interplay of events both within and among the components of the gonadal axis. Central to this axis are the gonadotropes, pituitary cells that synthesize and release the gonadotropins, LH and FSH. Of pivotal importance is the recognition that these trophic hormones, which are responsible for stimulating both the production of gonadal hormones and gametogenesis, are themselves secreted in a pulsatile fashion. Such pulsatile gonadotropin release reflects the integration of signals of both neural and gonadal origin that impinge upon the gonadotropes (Fig. 1). Indeed, the frequency with which the gonadotropins are released is believed in general to reflect the frequency with which quanta of GnRH are discharged by the hypothalamus, transported through the hypothalamic-hypophyseal portal circulation, and interact with appropriate receptors on responsive gonadotropes (1–6). The synthesis and secretion of GnRH itself are, in turn, modulated by catecholaminergic, serotoninergic, and opioid peptidergic as well as other neuromodulator systems within the hypothalamus and also by ambient concentrations of the gonadal hormones. Moreover, both in vitro and in vivo studies using the rat as a model have suggested that GnRH may feedback on itself via an ultrashort-loop system to inhibit its own secretion (7–9). Gonadotropin pulse amplitude may reflect both the amount of GnRH stimulating the gonadotrope and also the prevailing state of responsivity of the gonadotrope. Gonadotrope response characteristics appear to be a function not only of the neural signal, but also of the gonadal hormone milieu (10–23).
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism