Muscarinic stimulation increases Na+ entry in pancreatic B-cells by a mechanism other than the emptying of intracellular Ca2+ pools
(1996) Biochemical and Biophysical Research Communications — Vol. 224, n° 1, p. 67-73 (1996)
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- Stimulation of muscarinic (M3) receptors depolarizes pancreatic B-cells by increasing Na+ influx. Here, we measured [Na+]i and [Ca2+]i in B-cell clusters to investigate whether depletion of intracellular Ca2+ pools triggers this unusual transduction pathway for muscarinic receptors. Acetylcholine emptied Ca2+ pools less completely than did the SERCA pump inhibitors, thapsigargin, and cyclopiazonic acid. However, the rise in [Na+]i produced by acetylcholine was not mimicked by thapsigargin or cyclopiazonic acid and was not prevented by previous depletion of Ca2+ pools. Depolarization of B-cells by acetylcholine stimulates Ca2+ influx and steadily increases [Ca2+]i. In the presence of glucose and extracellular Ca2+, B-cells treated with thapsigargin or cyclopiazonic acid displayed large [Ca2+]i oscillations. Subsequent application of acetylcholine was followed by a sustained rise in [Ca2+]i as in untreated cells. In conclusion, intracellular Ca2+ pool depletion does not mediate acetylcholine stimulation of Na+ entry and of subsequent events. We propose that the muscarinic receptors are coupled to Na+ channels in B-cells.
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Miura, Y., Gilon, P., & Henquin, J.-C. (1996). Muscarinic stimulation increases Na+ entry in pancreatic B-cells by a mechanism other than the emptying of intracellular Ca2+ pools. Biochemical and Biophysical Research Communications, 224(1), 67-73. https://doi.org/10.1006/bbrc.1996.0985 (Original work published 1996)