GnRH is the key regulator of reproduction in the vertebrates. In this study, we investigated the release and synthesis of maturational gonadotropin hormone (GTH-II) stimulated by native GnRH forms, salmon GnRH (sGnRH) and chicken GnRH-II (cGnRH-II), in the goldfish pituitary. The experimental approach was to study the differences between desensitization induced by sGnRH and cGnRH-II administered in homologous and heterologous fashion. Pulsatile alternate treatments with sGnRH and cGnRH-II (i.e. sGnRH/cGnRH-II or cGnRH-II/sGnRH) at 10(-8) M (every 30 min) resulted in a lower degree of desensitization compared with homologous treatments with either sGnRH or cGnRH-II (sGnRH/sGnRH or cGnRH-II/cGnRH-II), or when combined together (sGnRH + cGnRH-II). We also investigated the effects of continuous treatments with sGnRH and cGnRH-II, administered in a homologous or heterologous fashion. Increasing concentrations of either sGnRH or cGnRH-II (10(-8)-10(-6) M) administered continuously (60 min) in a homologous fashion resulted in significant desensitization of the pituitary GTH-II release. Alternate continuous treatments with sGnRH and cGnRH-II (i.e. sGnRH/ cGnRH-II/sGnRH or cGnRH-II/sGnRH/cGnRH-II) resulted in lower degree of desensitization compared to homologous treatments, particularly at lower doses. We further investigated the effects of sGnRH and cGnRH-II on GTH-II beta and GTH-II alpha subunit messenger RNA (mRNA) levels in the goldfish pituitary. In sexually regressed animals, sGnRH treatment (4 mu g/fish) increased the accumulation of GTH-II beta and GTH-II alpha mRNA, whereas cGnRH-II treatment was without effect. In sexually mature animals, however, both cGnRH-II and sGnRH stimulated accumulation of GTH-II beta and GTH-II alpha mRNA, with cGnRH-II exerting a greater effect on GTH-II subunit mRNA production. These results suggest a differential control of GTH-II subunit gene expression or mRNA stabilization by sGnRH and cGnRH-II in the goldfish pituitary based on the stage of gonadal recrudescence. In general, the present findings support the hypothesis that sGnRH and cGnRH-II regulate the release and synthesis of GTH-II through different receptor-effector mechanisms in the goldfish pituitary.