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| 8: J Neuroendocrinol. 2003 Feb;15(2):204-14. |
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- A gonadotropin-releasing hormone insensitive,
thapsigargin-sensitive Ca2+ store reduces basal gonadotropin exocytosis and
gene expression: comparison with agonist-sensitive Ca2+ stores.
Johnson JD, Klausen C, Habibi H, Chang JP.
Department of Biological Sciences, University of Alberta, Edmonton, Alberta,
Canada.
We examined whether distinct Ca2+ 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-beta mRNA expression in
goldfish. Thapsigargin (Tg)-sensitive Ca2+ 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
Ca2+ 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-beta mRNA expression was decreased at 24 h by
2 microm Tg, and by inhibiting (10 microm Ry) and stimulating (1 nm Ry) Ry
receptors. Transient increases in GTH-II-beta mRNA were observed at 2 h and 12
h following 10 microm and 1 nm 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-beta mRNA expression. Our data show that GTH-II secretion,
storage and transcription can be independently controlled by distinct Ca2+
stores.
PMID: 12535163 [PubMed - indexed for MEDLINE]
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