INTRACELLULAR CA2-DERIVED PANCREATIC SOMATOSTATIN-SECRETING CELLS (QGP-1N)( SIGNALS IN HUMAN)

Citation
Pe. Squires et al., INTRACELLULAR CA2-DERIVED PANCREATIC SOMATOSTATIN-SECRETING CELLS (QGP-1N)( SIGNALS IN HUMAN), Pflugers Archiv, 428(3-4), 1994, pp. 275-282
Citations number
30
Categorie Soggetti
Physiology
Journal title
ISSN journal
00316768
Volume
428
Issue
3-4
Year of publication
1994
Pages
275 - 282
Database
ISI
SICI code
0031-6768(1994)428:3-4<275:ICPSC(>2.0.ZU;2-V
Abstract
Single-cell microfluorimetry techniques have been used to examine the effects of acetylcholine (0.1-100 mu M) on the intracellular free calc ium ion concentration ([Ca2+](i)) in a human-derived pancreatic somato statin-secreting cell line, QGP-1N. When applied to the bath solution, acetylcholine was found to evoke a marked and rapid increase in [Ca2](i) at all concentrations tested. These responses were either sustain ed, or associated with the generation of complex patterns of [Ca2+](i) transients. Overall, the pattern of response was concentration relate d. In general, 0.1-10 mu M acetylcholine initiated a series of repetit ive oscillations in cytoplasmic Ca2+, whilst at higher concentrations the responses consisted of a rapid rise in [Ca2+](i) followed by a sma ller more sustained increase. Without external Ca2+ 100 mu M acetylcho line caused only a transient rise in [Ca2+](i), whereas lower concentr ations of the agonist were able to initiate, but not maintain, [Ca2+]( i) oscillations. Acetylcholine-evoked Ca2+ signals were abolished by a tropine (1-10 mu M), verapamil (100 mu M) and caffeine (20 mM). Nifedi pine failed to have any significant effect upon agonist-evoked increas es in [Ca2+](i), whilst 50 mM KCl, used to depolarise the cell membran e, only elicited a transient increase in [Ca2+](i). Ryanodine (50-500 nM) and caffeine (1-20 mM) did not increase basal Ca2+ levels, but the Ca2+-ATPase inhibitors 2,5-di(tertbutyl)-hydroquinone (TBQ) and thaps igargin both elevated [Ca2+](i) levels. These data demonstrate for the first time cytosolic Ca2+ signals in single isolated somatostatin-sec reting cells of the pancreas. We have demonstrated that acetylcholine will evoke both Ca2+ influx and Ca2+ mobilisation, and we have partial ly addressed the subcellular mechanism responsible for these events.