Dopaminergic regulation of pituitary gonadotrophin-releasing hormone receptor activity in the goldfish (Carassius auratus)

Abstract

In goldfish, dopamine acts as an endogenous inhibitor of basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release. The purpose of the present study was to investigate the effects of dopamine on the pituitary GnRH receptors in vivo and in vitro in goldfish. The goldfish pituitary contains two classes of GnRH-binding sites, a high-affinity/low-capacity site and low-affinity/high-capacity site. Injection of domperidone, a dopamine antagonist, resulted in a dose- and time-related increase in capacity of both the high- and low-affinity GnRH-binding sites; apomorphine, a dopamine agonist, completely reversed this effect. The effects on GnRH receptor capacity correlated very closely with changes in serum gonadotrophin concentrations. Domperidone was generally without effect on GnRH-binding affinity; however, a small but significant decrease in affinity was observed for the low-affinity binding site at 18 h after injection of the highest dose of domperidone used (40 mumol/kg body weight). Treatment with apomorphine of goldfish pituitary fragments in a perifusion system caused a decrease in the capacity of both the high- and low-affinity GnRH-binding sites without affecting binding affinity; domperidone reversed this effect. It is concluded that the dopaminergic inhibition of basal and GnRH-stimulated gonadotrophin release in goldfish might, in part, be the result of a down-regulation of the pituitary GnRH receptors; this effect of dopamine can be achieved by a direct action at the pituitary level.