title: Calcium signaling and gonadotropin secretion.
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.
authors.affiliation: Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Building 10, Rm. 8C407, Bethesda, MD 20892, USA.
authors.forename: K J
authors.initials: KJ
authors.lastname: Catt
authors.forename: S S
authors.initials: SS
authors.lastname: Stojilković