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Intracellular Calcium Involvement in Pituitary Adenylate Cyclase‐Activating Polypeptide Stimulation of Growth Hormone and Gonadotrophin Secretion in Goldfish Pituitary Cells
Author(s) -
Sawisky G. R.,
Chang J. P.
Publication year - 2005
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 - 10.1111/j.1365-2826.2005.01312.x
Subject(s) - medicine , endocrinology , thapsigargin , ryanodine receptor , cyclopiazonic acid , pituitary adenylate cyclase activating peptide , serca , biology , dantrolene , inositol , phospholipase c , chemistry , calcium , receptor , atpase , biochemistry , neuropeptide , vasoactive intestinal peptide , enzyme
The involvement of intracellular Ca 2+ stores and their regulatory mechanisms in mediating pituitary adenylate cyclase‐activating polypeptide (PACAP) stimulation of growth hormone (GH) and maturational gonadotrophin (GTH‐II) secretion from goldfish pituitary cells was investigated using a cell column perifusion system. Pretreatment with caffeine abolished the GH and GTH‐II responses to PACAP. Dantrolene attenuated PACAP‐elicited GTH‐II release but did not affect the GH response, whereas ryanodine and 8‐bromo‐cADP ribose did not alter PACAP‐induced GH and GTH‐II release. Two endoplasmic/sarcoplasmic reticulum Ca 2+ ATPase (SERCA) inhibitors, thapsigargin and cyclopiazonic acid, augmented PACAP‐induced GTH‐II release; similarly, thapsigargin elevated GH responses to PACAP. Treatment with carbonyl cyanide m ‐chlorophenylhydrazone, a mitochondrial uncoupler, reduced PACAP‐stimulated GH release; however, inhibition of the mitochondrial Ca 2+ uniport by Ru360 did not affect GH and GTH‐II responses. The phosphatidyl inositol (PI)‐specific phospholipase C (PLC) inhibitor ET‐18‐OCH 3 inhibited, whereas the phosphatidyl‐choline (PC)‐specific PLC inhibitor D609 enhanced, PACAP‐stimulated GH and GTH‐II responses. On the other hand, the IP 3 receptor blocker xestospongin D had no effect on PACAP‐induced GTH‐II response and potentiated the GH response. These results suggest that, despite some differences between GH and GTH‐II cells, PACAP actions in both cell types generally rely on a caffeine‐sensitive, but a largely ryanodine receptor‐independent, mechanism. PC‐PLC and some SERCA negatively modulate PACAP actions but mitochondrial Ca 2+ stores per se are not important. A novel PI‐PLC mechanism, which does not involve the traditional IP 3 /Ca 2+ pathway, is also suggested.