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Differences in Gonadotropin-Releasing Hormone-Induced Calcium Signaling between Melatonin-Sensitive and Melatonin-Insensitive Neonatal Rat Gonadotrophs¹

Hana Zemková and JiÍ VanEK

Institute of Physiology, Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic

Address all correspondence and requests for reprints to: Hana Zemková, Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenská 1083, 142 20 Prague 4, Czech Republic. E-mail: zemkova{at}biomed.cas.cz

The sensitivity of GnRH-stimulated calcium signaling to melatonin, in a subpopulation of neonatal gonadotrophs, is supposed to be attributable to melatonin receptors. However, it is not yet known whether the intracellular pathway for GnRH action in melatonin-sensitive cells is the same as in melatonin-insensitive cells. By monitoring intracellular Ca²⁺ changes as an outward current carried through apamin-sensitive Ca²⁺-activated K⁺ channels, we compared GnRH-induced calcium responses in these two subpopulations of neonatal gonadotrophs. GnRH induced various oscillatory, as well as nonoscillatory, responses in both cell types that was not related to melatonin sensitivity. Melatonin-sensitive GnRH-induced responses could be clearly distinguished according to the pharmacological properties of their latency. The latency increased in zero extracellular Ca²⁺ or with the addition of nifedipine, staurosporine, and ryanodine. This effect was only rarely observed in melatonin-insensitive cells. This indicates that there are two pathways for initiation of GnRH-induced calcium signaling in neonatal gonadotrophs. The first pathway is mediated by inositol 1,4,5,-trisphosphate production, whereas the second involves extracellular calcium entry through voltage-dependent L-type Ca²⁺ channels, protein kinase C activation, and Ca²⁺ release from a ryanodine-sensitive store, which may coactivate Ca²⁺ release from an inositol 1,4,5,-trisphosphate-sensitive store. Only the second mechanism is accessible to inhibition by melatonin.