In several teleost species, including the African catfish, dopamine acts as an endogenous inhibitor of gonadotropin-releasing hormone (GnRH)-stimulated gonadotropin (GTH) release. The present in vivo study was carried out to investigate whether this inhibitory action of dopamine can be explained by an effect on the pituitary GnRH receptors. To that end, sexually mature female catfish were treated with dopamine and the dopamine antagonist pimozide (PIM), respectively. At different time intervals after injection, the pituitaries were collected, and in a GnRH receptor assay the GnRH-binding parameters were determined. The dopamine treatment affected neither GnRH-binding capacity nor affinity. The PIM treatment resulted in a two-fold increase in pituitary GnRH-binding capacity without affecting binding affinity. The time course of this effect coincided with the potentiating effect of PIM of the GTH-releasing activity of a GnRH analog. It is concluded that the stimulatory effect of PIM on the action of GnRH might, in part, be due to an increased pituitary GnRH-binding capacity. Reversely, these results suggest that the endogenous dopaminergic inhibition of GnRH-stimulated GTH release may be mediated, at least in part, through down-regulation of the pituitary GnRH receptors.
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