PMID- 21153267 OWN - NLM STAT- PubMed-not-MEDLINE DCOM- 20121002 LR - 20211020 IS - 1355-008X (Print) IS - 1355-008X (Linking) VI - 4 IP - 2 DP - 1996 Apr TI - Spontaneous and agonist-induced calcium oscillations in single human nonfunctioning adenoma cells. PG - 123-32 LID - 10.1007/BF02782757 [doi] AB - The effects of gonadotropin-releasing hormone (GnRH) and GnRH-associated peptide (GAP) on cytosolic free calcium concentration ([Ca(2+)](i)) were investigated in 20 human nonfunctioning pituitary adenomas. We divided these tumors into three classes according to their response pattern to hypothalamic peptides. In type I adenomas (8 out of 20 adenomas), GnRH and GAP mobilized intracellular calcium ions stored in a thapsigargin (TG)-sensitive store. For the same concentration of agonist, two distinct patterns of GnRH-GAP-induced Ca(2+) mobilization were observed (1) sinusoidal oscillations, and (2) monophasic transient. The latter is followed by a protein kinase C (PKC)-dependent increase in calcium influx through L-type channels. In type II adenomas (7 out of 20 adenomas), GnRH and GAP only stimulate calcium influx through dihydropyridine-sensitive Ca(2+) channels by a PKC-dependent mechanism. TG (1 muM) did not affect [Ca(2+)](i) in these cells, suggesting that they do not possess TG-sensitive Ca(2+) pools. All the effects of GnRH and GAP were blocked by an inhibitor of phospholipase C (PLC), suggesting that they were owing to the activation of the phosphoinositide turnover. Type I and type II adenoma cells showed spontaneous Ca(2+) oscillations that were blocked by dihydropyridines and inhibition of PKC activity. GnRH and GAP had no effect on the [Ca(2+)](i) of type III adenoma cells that were also characterized by a low resting [Ca(2+)](i) and by the absence of spontaneous Ca(2+) fluctuations. K(+)-induced depolarization provoked a reduced Ca(2+) influx, whereas TG had no effect on the [Ca(2+)](i) of type III adenoma cells. The variety of [Ca(2+)](i) response patterns makes these cells a good cell model for studying calcium homeostasis in pituitary cells. FAU - Vacher, P AU - Vacher P AD - Laboratoire de Neurophysiologie, CNRS URA 1200, Universite de Bordeaux 2, 146 rue Leo Saignat, PB 22, 33076, Bordeaux Cedex, France. FAU - Bresson-Bepoldin, L AU - Bresson-Bepoldin L FAU - Dufy-Barbe, L AU - Dufy-Barbe L FAU - Odessa, M F AU - Odessa MF FAU - Guerin, J AU - Guerin J FAU - Dufy, B AU - Dufy B LA - eng PT - Journal Article PL - United States TA - Endocrine JT - Endocrine JID - 9434444 EDAT- 1996/04/01 00:00 MHDA- 1996/04/01 00:01 CRDT- 2010/12/15 06:00 PHST- 1995/07/06 00:00 [received] PHST- 1996/01/17 00:00 [accepted] PHST- 1995/11/14 00:00 [revised] PHST- 2010/12/15 06:00 [entrez] PHST- 1996/04/01 00:00 [pubmed] PHST- 1996/04/01 00:01 [medline] AID - 10.1007/BF02782757 [doi] PST - ppublish SO - Endocrine. 1996 Apr;4(2):123-32. doi: 10.1007/BF02782757.