DOPAMINE-D-2 ACTIONS ON VOLTAGE-DEPENDENT CALCIUM CURRENT AND GONADOTROPIN-II SECRETION IN CULTURED GOLDFISH GONADOTROPHS

Dopamine D-2-receptor activation directly inhibits GnRH-induced gonado tropin-II (maturational gonadotropin, GTH-II) secretion from goldfish pituitary cells. In this study, we show that dopamine and its D-2 agon ist, quinpirole, reduced GTH-II secretion induced by either high extra cellular K+ concentration or the voltage-gated Ca2+ channel agonist, B ay K 8644. These actions of dopamine were blocked by addition of the d opamine D-2-receptor antagonist, spiperone. The actions of dopamine on Ca2+ current in single identified goldfish gonadotrophs were assessed in voltage-clamp experiments using Ba2+ as the charge carrier through voltage-gated Ca2+ channels. Dopamine caused a concentration-dependen t reduction in Ba2+ current amplitude with an EC50 of 1.0 +/- 0.3 nM, but did not shift the current-voltage relationship. The D-2 agonist qu inpirole also caused a dose-dependent reduction in the Ba2+ current am plitude with an EC50 of 2.7 +/- 1.4 nM. Quinpirole slowed the activati on and inactivation kinetics, as well as removing the steady-state ina ctivation properties of the Ba2+ current. In contrast to the actions o f quinpirole, the dopamine D-1-receptor agonist, SKF 38393, did not af fect the Ba2+ current. The inhibitory action of dopamine on voltage-de pendent Ca2+ currents was reversed by spiperone, but not by the D-1 an tagonist SKF 83566. Voltage-dependent Na+ and K+ currents were not aff ected by dopamine or dopamine agonists. These data indicate that dopam ine D-2-receptor activation reduces Ca2+ influx through voltage-depend ent Ca2+ channels to inhibit GTH-II secretion.