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A Gonadotropin‐Releasing Hormone Insensitive, Thapsigargin‐Sensitive Ca 2+ Store Reduces Basal Gonadotropin Exocytosis and Gene Expression: Comparison with Agonist‐Sensitive Ca 2+ Stores
Author(s) -
Johnson J. D.,
Klausen C.,
Habibi H.,
Chang J. P.
Publication year - 2003
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.2003.00977.x
Subject(s) - medicine , endocrinology , thapsigargin , gonadotropin , gonadotropin releasing hormone , biology , chemistry , receptor , hormone , luteinizing hormone , calcium
We examined whether distinct Ca 2+ stores differentially control basal and gonadotropin (GTH‐II)‐releasing hormone (GnRH)‐evoked GTH‐II release, long‐term GTH‐II secretion and contents, and GTH‐II‐ β mRNA expression in goldfish. Thapsigargin (Tg)‐sensitive Ca 2+ stores mediated neither caffeine‐evoked GTH‐II release, nor salmon (s)GnRH‐ and chicken (c)GnRH‐II‐stimulated secretion; the latter responses were previously shown to involve ryanodine (Ry)‐sensitive Ca 2+ stores. Surprisingly, Tg decreased basal GTH‐II release. This response was attenuated by prior exposure to sGnRH and caffeine, but was insensitive to the phosphatase inhibitor okadaic acid, the inhibitor of constitutive release brefeldin A and cGnRH‐II. GTH‐II‐ β mRNA expression was decreased at 24 h by 2 µ m Tg, and by inhibiting (10 µ m Ry) and stimulating (1 n m Ry) Ry receptors. Transient increases in GTH‐II‐ β mRNA were observed at 2 h and 12 h following 10 µ m and 1 n m Ry treatment, respectively. Effects of Tg, Ry and GnRH on long‐term GTH‐II secretion, contents and apparent production differed from one another, and these changes were not well correlated with changes in GTH‐II‐ β mRNA expression. Our data show that GTH‐II secretion, storage and transcription can be independently controlled by distinct Ca 2+ stores.