INVOLVEMENT OF EXTRACELLULAR-SODIUM IN AGONIST-INDUCED GONADOTROPIN-RELEASE FROM GOLDFISH (CARASSIUS-AURATUS) GONADOTROPHS

In goldfish, gonadotropin (GTH-II) responses to the two endogenous GnR Hs, salmon-GnRH and chicken-GnRH-II, are mediated by activation of pro tein kinase C (PKC) and voltage-sensitive Ca2+ channels. In this study , we investigated the role of extracellular Na+, voltage-dependent Na channels, and the plasma membrane Na+/H+ exchanger in mediating GnRH- stimulated GTH-II release from dispersed goldfish pituitary cells. Per ifusion with Na+-depleted medium reduced the GTH-II response to both G nRHs and the response to the protein kinase C activator, phorbol 12-my ristate 13-acetate. Conversely, increasing Na+ influx with veratridine (100 mu M) stimulated GTH-II release in the presence and in the absen ce of extracellular Ca2+. However, the voltage-sensitive Na+ channel b locker, tetrodotoxin (1 mu M), did not affect GnRH-stimulated GTH-II r elease, and the GnRHs did not affect voltage-sensitive Na+ currents. I n contrast, the Na+/H+ antiport inhibitors, amiloride or its analog, D MA, reduced GTH-II responses to the GnRHs and phorbol la-myristate 13- acetate. The Na+/H+ antiport inhibitors did not affect voltage-sensiti ve Ca2+ or Na+ currents or the GTH-II release response to the Ca2+ ion ophore, ionomycin. These findings indicate that extracellular Na+ and the Na+/H+ exchanger are involved in the mediation of GnRH-stimulated GTH-II release. In addition, Na+ entry may modulate GTH-II release ind ependent of extracellular Ca2+.