ISSN:
1432-2013
Keywords:
Somatostatin
;
Intracellular Ca2+ homeostasis
;
Somatostatin-secreting cell
;
Fura-2
;
Microfluorimetry
;
[Ca2+]i
;
QGP-1N cells
;
Acetylcholine
;
Thapsigargin
;
Caffeine
;
Ryanodine
;
Islets of Langerhans
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00724507
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