Multiplicity of gonadotropin-releasing hormone signaling: a comparative perspective.

GnRH regulation of GtH synthesis and release involves PKC- and Ca(2+)-dependent pathways. There are differential signaling mechanisms in different cells, tissues and species. Signaling mechanisms involved in GnRH-mediated GtH release appear to be more conserved compared to that of GnRH-induced GtH gene expression. This may in part be due to different 5' regulatory regions on the GtH-subunit genes. Cell type specific expression of various signaling and/or exocytotic components may also be responsible for the observed differences in signaling between gonadotropes and somatotropes in the goldfish and tilapia pituitaries. However, this can not explain the observed differences in post receptor mechanisms for sGnRH and cGnRH-II in gonadotropes which is more likely to result from the existence of GnRH receptor subtypes. Support for this hypothesis is also provided by observations on mechanisms of autocrine/paracrine regulation of ovarian function by sGnRH and cGnRH-II in the goldfish ovary in which GnRH antagonists only block GnRH stimulation of oocyte meiosis and do not affect inhibitory effects of sGnRH. It should be easier to explain observed variations concerning GnRH-induced responses as more information becomes available on different types of GnRH receptors, and their distribution and function in mammals and non-mammalian vertebrates.