Nitric oxide signaling in ghrelin-induced LH release from goldfish pituitary cells.
Dopamine D2-receptor activation directly inhibits GnRH-induced gonadotropin-II (maturational gonadotropin, GTH-II) secretion from goldfish pituitary cells. In this study, we show that dopamine and its D2 agonist, quinpirole, reduced GTH-II secretion induced by either high extracellular K+ concentration or the voltage-gated Ca2+ channel agonist, Bay K 8644. These actions of dopamine were blocked by addition of the dopamine D2-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-dependent reduction in Ba2+ current amplitude with an EC50 of 1.0+/-0.3 nM, but did not shift the current-voltage relationship. The D2 agonist quinpirole also caused a dose-dependent reduction in the Ba2+ current amplitude with an EC50 of 2.7+/-1.4 nM. Quinpirole slowed the activation and inactivation kinetics, as well as removing the steady-state inactivation properties of the Ba2+ current. In contrast to the actions of quinpirole, the dopamine D1-receptor agonist, SKF 38393, did not affect the Ba2+ current. The inhibitory action of dopamine on voltage-dependent Ca2+ currents was reversed by spiperone, but not by the D1 antagonist SKF 83566. Voltage-dependent Na+ and K+ currents were not affected by dopamine or dopamine agonists. These data indicate that dopamine D2-receptor activation reduces Ca2+ influx through voltage-dependent Ca2+ channels to inhibit GTH-II secretion.