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Voltage-dependent InsP3-insensitive calcium channels in membranes of pancreatic endoplasmic reticulum vesicles

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Schmid,  Andreas
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Dehlinger-Kremer,  Martine
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Schulz,  Irene
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Gögelein,  Heinz
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Citation

Schmid, A., Dehlinger-Kremer, M., Schulz, I., & Gögelein, H. (1990). Voltage-dependent InsP3-insensitive calcium channels in membranes of pancreatic endoplasmic reticulum vesicles. Nature, 346(6282), 374-376. doi:10.1038/346374a0.


Cite as: http://hdl.handle.net/21.11116/0000-0007-F116-0
Abstract
Stimulus-secretion coupling in exocrine glands involves Ca2+ release from intracellular stores. In endoplasmic reticulum vesicle preparations from rat exocrine pancreas, an inositol 1,4,5-trisphosphate(InsP3)-sensitive, as well as an InsP3-insensitive, Ca2+ pool has been characterized. But Ca2+ channels in the endoplasmic reticulum of rat exocrine pancreas have not been demonstrated at the level of single-channel current. We have now used the patch-clamp technique on endoplasmic reticulum vesicles fused by means of the dehydration-rehydration method. In excised patches, single Ba2+- and Ca2+-selective channels were recorded. The channel activity was markedly voltage-dependent. Caffeine increased channel open-state probability, whereas ruthenium red and Cd2+ blocked single-channel currents. Ryanodine, nifedipine and heparin had no effect on channel activity. The channel activity was not dependent on the free Ca2+ concentration, the presence of InsP3, or pH. We conclude that this calcium channel mediates Ca2+ release from an intracellular store through an InsP3-insensitive mechanism.