Calcium signaling and gonadotropin secretion
1Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Building 10, Rm. 8C407, Bethesda, MD 20892, USA.
Abstract:
Agonist activation of pituitary gonadotrophs by gonadotropin-releasing hormone (GnRH) stimulates rapid InsP(3)-dependent peaks of calcium mobilization and luteinizing hormone (LH) release, followed by sustained increases in calcium-influx and hormone secretion. Receptor-mediated calcium entry through L-type and dihydropyridine-insensitive calcium channels accounts for the sustained elevation of cytosolic calcium during GnRH action, and for most of the gonadotropin secretory response. Protein kinase C contributes to the phase of sustained LH release from GnRH-stimulated gonadotrophs, and also to gonadotropin synthesis. Calcium-dependent inactivation of L channels occurs during GnRH action, and appears to be a primary factor in the onset of desensitization of gonadotropin secretion.
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