GTH I and GTH II secretion profiles during the reproductive cycle in female rainbow trout: relationship with pituitary responsiveness to GnRH-A stimulation.

The recent purification of two gonadotropins, GTH I and GTH II, in teleost fish and the development of their specific radioimmunoassays using antibodies directed against their beta subunits have demonstrated that earlier assays for GTH II also measured GTH I. Most of the results on the gonadotropic control of reproduction in fish must thus be reinvestigated using specific assays for each gonadotropin. The present investigation examines changes in blood plasma levels of GTH I and GTH II during the annual reproductive cycle of rainbow trout in relation to the ability of gonadotropin-releasing hormone (GnRH) to stimulate in vivo GTH I and GTH II secretion, with focus on the periovulatory period. GTH I was detected from immature to postovulatory stages, with a significant increase at the onset of exogenous vitellogenesis, with GTH I levels rising from 7.83 +/- 3.37 to 16.87 +/- 4.52 ng/ml. GTH II remained very low until the end of the vitellogenesis. For both hormones, the most significant variations were measured during the periovulatory period. GTH II levels peaked on the day of maturation, but the increase was biphasic with a first peak arising 4 days prior to maturation. This evaluation of GTH II was preceded by a progressive and significant rise GTH I levels starting from 5.83 +/- 2.17 ng/ml 8 days before maturation and increasing to more than 10 ng/ml on the day of maturation. Thus, the GTH II maturation surge is not the only gonadotropic signal occurring before ovulation. The role of the preovulatory GTH I increase remains unknown. After ovulation the secretory profiles of the two hormones depended on the presence of absence of ovulated eggs in the body cavity. There was a major increase in GTH I levels starting 4 days after ovulation and egg stripping, reaching more than 25 ng/ml. Conversely, in these fish the GTH II levels gradually decreased. In the fish which kept their eggs in the body cavity the progress was reversed; 8 days after maturation, GTH II increased to levels similar to those measured prior to maturation; the presence of the eggs prevented an increase in GTH I. This seems to indicate that postovulatory regulation of GTH I and GTH II secretion might involve ovarian factors that act in an antagonistic fashion. The prevention of the increase in GTH I levels in the presence of eggs suggests that as long as eggs are present in the body cavity, the development of a new cycle of gametogenesis is not possible, since GTH I is the gonadotropin mainly involved in controlling this phenomena. GnRH cannot significantly stimulate GTH I secretion at any stage of gametogenesis, even when its levels increased after ovulation. Other factors antagonizing GnRH are involved. The well-known antagonistic effect of dopamine on the GnRH stimulated GTH II secretion is fish is not involved since the dopamine antagonist, pimozide, was ineffective in inducing a stimulatory action of GnRH on GTH I secretion. Although GnRH can stimulate GTH II secretion from mid-vitellogenesis, the response to GnRH was not correlated with GTH II in blood. These results suggest that GTH I and GTH II secretions are regulated by different mechanisms and different factors.