Ghrelin stimulation of gonadotropin (LH) release from goldfish pituitary cells: presence of the growth hormone secretagogue receptor (GHS-R1a) and involvement of voltage-sensitive Ca2+ channels.

Ghrelin (GRLN) stimulates maturational gonadotropin (LH) secretion in goldfish. This study identified GRLN receptors (GHS-Rs) in goldfish tissues and examined the involvement of voltage-sensitive Ca(2+) channels (VSCCs) in ghrelin action. A partial goldfish GHS-R1a sequence was obtained and expression observed in brain, pituitary, spleen, kidney, heart, gill, ovary, testis, and intestine. Synthetic goldfish GRLN (gGRLN(19)) stimulated LH secretion from dispersed goldfish pituitary cells in column perifusion and increased intracellular Ca(2+) (Ca(2+)) in identified goldfish gonadotropes. gGRLN(19) did not stimulate LH secretion either in the presence of Ca(2+)-free media, or the L-type VSCC inhibitors nifedipine and verapamil. Similarly, gGRLN(19)-elicited increases in Ca(2+) were attenuated by Ca(2+)-free media and nifedipine. Furthermore, when LH release and Ca(2+) were elevated by Bay K8644, gGRLN(19) had no further effect. These results indicate that GHS-R1a is present in goldfish pituitary and Ca(2+) entry through VSCC mediates direct gGRLN(19) action on LH release in goldfish pituitary cells.