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Cytoplasmic calcium transients due to single action potentials and voltage-clamp depolarizations in mouse pancreatic B-cells.
Authors:P Rorsman  C Amml  P O Berggren  K Bokvist  and O Larsson
Affiliation:Department of Medical Biophysics, Gothenburg University, Sweden.
Abstract:Changes in the cytoplasmic free calcium concentration (Ca2+]i) in pancreatic B-cells play an important role in the regulation of insulin secretion. We have recorded Ca2+]i transients evoked by single action potentials and voltage-clamp Ca2+ currents in isolated B-cells by the combination of dual wavelength emission spectrofluorimetry and the patch-clamp technique. A 500-1000 ms depolarization of the B-cell from -70 to -10 mV evoked a transient rise in Ca2+]i from a resting value of approximately 100 nM to a peak concentration of 550 nM. Similar Ca2+]i changes were associated with individual action potentials. The depolarization-induced Ca2+]i transients were abolished by application of nifedipine, a blocker of L-type Ca2+ channels, indicating their dependence on influx of extracellular Ca2+. Following the voltage-clamp step, Ca2+]i decayed with a time constant of approximately 2.5 s and summation of Ca2+]i occurred whenever depolarizations were applied with an interval of less than 2 s. The importance of the Na(+)-Ca2+ exchange for B-cell Ca2+]i maintenance was evidenced by the demonstration that basal Ca2+]i rose to 200 nM and the magnitude of the depolarization-evoked Ca2+]i transients was markedly increased after omission of extracellular Na+. However, the rate by which Ca2+]i returned to basal was not affected, suggesting the existence of additional Ca2+]i buffering processes.
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