PMID: 18411081Sep 1, 1989Paper

Calcium signaling and gonadotropin secretion

Trends in Endocrinology and Metabolism : TEM
K J Catt, S S Stojilković

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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Citations

Sep 1, 1991·Molecular and Cellular Endocrinology·Z Naor
Apr 1, 1991·Molecular and Cellular Endocrinology·J DavidsonR P Millar
Jan 1, 1993·Molecular and Cellular Endocrinology·A PetitS Bélisle
Sep 1, 1992·Trends in Endocrinology and Metabolism : TEM·K Gordon, G D Hodgen
Dec 16, 1997·Proceedings of the National Academy of Sciences of the United States of America·H FanJ A Wright
Nov 26, 1996·Proceedings of the National Academy of Sciences of the United States of America·H FanJ A Wright

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