Novel, thapsigargin-insensitive intracellular Ca(2+) stores control growth hormone release from goldfish pituitary cells

• Published in: Molecular and cellular endocrinology 2000-07, Vol.165 (1-2), p.139-150
• Main Authors: Johnson, J D, Chang, J P
• Format: Article
• Language: English
• Subjects: Animals; Caffeine - pharmacology; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Calcium Signaling; Cells, Cultured; Gallic Acid - analogs & derivatives; Gallic Acid - pharmacology; Goldfish; Growth Hormone - metabolism; Intracellular Fluid - metabolism; Models, Biological; Pituitary Gland - cytology; Pituitary Gland - drug effects; Pituitary Gland - physiology; Thapsigargin - pharmacology
• ISSN: 0303-7207
• DOI: 10.1016/S0303-7207(00)00252-5

The relative contribution of intracellular Ca(2+) stores to basal and agonist-stimulated hormone release in pituitary cells is still not well understood, especially in non-mammalian vertebrates. Using ratiometric Ca(2+) imaging of single identified goldfish somatotropes, along with time-resolved measurements of growth hormone (GH) secretion, we investigated the Ca(2+)-dependent signal transduction of two endogenous regulators of GH release from the goldfish pituitary. Two gonadotropin-releasing hormones (sGnRH and cGnRH-II) initiated GH release in nominally Ca(2+) free conditions. GnRH-evoked GH release was additive to KCl-stimulated GH responses. Ca(2+) signals and GH release elicited by both GnRHs were abolished by pretreatment with TMB-8, which blocks the release of Ca(2+) from intracellular stores. GnRH-stimulated GH secretion is mediated by caffeine-sensitive intracellular Ca(2+) stores that are functionally independent from those sensitive to thapsigargin and other inhibitors of SERCA-type Ca(2+)/ATPases. The caffeine/TMB-8-sensitive Ca(2+) stores are also involved in spontaneous Ca(2+) signalling and the maintenance of prolonged GH release.