Novel, thapsigargin-insensitive intracellular Ca2+ stores control growth hormone release from goldfish pituitary cells

The relative contribution of intracellular Ca2+ stores to basal and agonist-stimulated hormone release in pituitary cells is still not well understood, especially in non-mammalian vertebrates. Using ratiometric Ca2+ imaging of single identified goldfish somatotropes, along with time-resolved measurements of growth hormone (GH) secretion, we investigated the Ca2+-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 Ca2+ free conditions. GnRH-evoked GH release was additive to KCl-stimulated GH responses. Ca2+ signals and GH release elicited by both GnRHs were abolished by pretreatment with TMB-8, which blocks the release of Ca2+ from intracellular stores. GnRH-stimulated GH secretion is mediated by caffeine-sensitive intracellular Ca2+ stores that are functionally independent from those sensitive to thapsigargin and other inhibitors of SERCA-type Ca2+/ATPases. The caffeine/TMB-8-sensitive Ca2+ stores are also involved in spontaneous Ca2+ signalling and the maintenance of prolonged GH release. (C) 2000 Published by Elsevier Science Ireland Ltd. All rights reserved.