Direct action of GnRH variants on goldfish oocyte meiosis and follicular steroidogenesis

Abstract

This study investigated the effects of gonadotropin-releasing hormones (GnRH) present in the goldfish brain (sGnRH and cGnRH-II) as well as a number of other GnRH variants on the reinitiation of meiosis and testosterone production in the follicle-enclosed goldfish oocytes, in vitro. All GnRH peptides tested individually stimulated oocyte meiosis in vitro, as determined by germinal vesicle breakdown (GVBD) as well as histone H1 kinase activity, which is an indicator of maturation promoting factor (MPF) production. The GnRH peptides tested had no detectable effect on basal follicular testosterone production with the exception of lGnRH-III, which had a relatively small stimulatory effect. In the presence of gonadotropin hormone (GTH), however, both sGnRH and lGnRH-III inhibited GTH-induced meiosis and steroidogenesis, whereas other GnRH peptides had no effect on GTH-induced responses. Addition of a GnRH antagonist effectively blocked the stimulatory effect of all GnRH peptides on oocyte meiosis, but was without effect on the inhibitory actions of sGnRH and lGnRH-III on GTH-induced meiosis, suggesting the involvement of different pathways mediating the stimulatory and inhibitory actions of sGnRH and lGnRH-III. These GnRH peptides were found to bind to the GnRH receptors in the goldfish ovary with different affinities (equilibrium association constant, K a). The findings provide novel information on the activity of GnRH variants in the goldfish ovary and provide a strong support for the hypothesis that GnRH plays a paracrine/autocrine role in the regulation of ovarian function in goldfish.