Lack of involvement of arachidonic acid metabolism in chicken gonadotropin releasing hormone ii cgnrh ii stimulation of gonadotropin secretion in dispersed pituitary cells of goldfish carassius auratus identification of a major difference in salmon gnrh and chicken gnrh ii mechanisms of action
Chang, J.P.; Wildman, B.; Van Goor, F.
Molecular and Cellular Endocrinology 79(1-3): 75-84
Gonadotropin (GTH) release in static incubations of dispersed goldfish pituitary cells was stimulated by chicken GTH-releasing hormone II (cGNRH-II), salmon (s)GnRH, phospholipase A2, phospholipase C, phospholipase D, and arachidonic acid (AA). Coincubation with nordihydroguaiarectic acid (NDGA), 5,8,11,14-eicosatetraeonic acid, and indomethacin did not alter the GTH responses to cGnRH-II. In contrast, NDGA reduced sGnRH-stimulated GHT release. Incubation with Ca2+-deficient medium abolished the GTH responses to cGn-RH-II, reduced sGnRH-stimulated GHT release, but did not alter AA-actions on GTH secretion. Apomorphine, a dopamine agonists that had been shown to partially inhibit the GTH responses to sGnRH and to abolish those induced by cGn-RH-II, did not affect the hormone response to AA. However, the partial inhibitory actions of NDGA and apomorphine on sGnRH-induced GTH release was additive. These findings suggest the existence of a major difference in cGnRH-II and SGnRH stimulation of GTH release - AA metabolism is not involved in cGnRH-II, as opposed to sGnRH actions. This difference in second messenger activation may also explain the differential sensitivity of the two GnRH peptides to dopamine inhibition and manipulations of extracellular Ca2+ availability. The results further suggest that dopamine and AA affect GTH release via non-overlapping signal transduction pathways.