Intracellular Ca2+ signals in human-derived pancreatic somatostatin-secreting cells (QGP-1N)

Single-cell microfluorimetry techniques have been used to examine the effects of acetylcholine (0.1-100 μM) on the intracellular free calcium ion concentration (Ca2+i) in a human-derived pancreatic somatostatin-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 sustained, or associated with the generation of complex patterns of Ca2+i transients. Overall, the pattern of response was concentration related. In general, 0.1-10 μM acetylcholine initiated a series of repetitive oscillations in cytoplasmic Ca2+, whilst at higher concentrations the responses consisted of a rapid rise in Ca2+i followed by a smaller more sustained increase. Without external Ca2+, 100 μM acetylcholine caused only a transient rise in Ca2+i, whereas lower concentrations of the agonist were able to initiate, but not maintain, Ca2+i oscillations. Acetylcholine-evoked Ca2+ signals were abolished by atropine (1-10 μM), verapamil (100 μM) and caffeine (20 mM). Nifedipine failed to have any significant effect upon agonist-evoked increases in Ca2+i, whilst 50 mM KCl, used to depolarise the cell membrane, 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(tert-butyl)-hydroquinone (TBQ) and thapsigargin both elevated Ca2+i levels. These data demonstrate for the first time cytosolic Ca2+ signals in single isolated somatostatin-secreting cells of the pancreas. We have demonstrated that acetylcholine will evoke both Ca2+ influx and Ca2+ mobilisation, and we have partially addressed the subcellular mechanism responsible for these events. © 1994 Springer-Verlag