PMID: 8603090Mar 13, 1996Paper

A possible role of the ATP-sensitive potassium ion channel in determining the duration of spike-bursts in mouse pancreatic beta-cells

Biochimica Et Biophysica Acta
W G DingH Kitasato

Abstract

The pancreatic beta-cell displays an electrical activity consisting of spike bursts and silent phases at glucose concentrations of about 10 mM. The mechanism of initial depolarization induced by glucose is well defined. However, the mechanism inducing the silent phase has not been fully elucidated. In the present study, the possibility of involvement of ATP-sensitive K+ channels in repolarization was examined using the patch-clamp technique in the cell-attached recording configuration. Ouabain (0.1 mM), an inhibitor of Na+/K+-ATPase, caused a complete suppression of ATP-sensitive K+ channel activity followed by typical biphasic current deflections, which were due to action potentials. The channel activity was also inhibited by removal of K+ from a perifusion solution. Furthermore, the activity of ATP-sensitive K+ channels was markedly inhibited either by replacement of external NaCl with LiCl or by addition of amiloride (0.2 mM), a blocker of Na+/H+ antiport. Addition of L-type Ca2+ channel blockers such as Nifedipine for Mn2+ induced the complete suppression of K+ channel activity. These findings strongly suggest that a fall in ATP consumption results in sustained depolarization, and that the repolarizations interposed between...Continue Reading

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Citations

Oct 17, 2003·Neuromuscular Disorders : NMD·Domenico TricaricoDiana Conte Camerino
Mar 23, 2011·Reproductive Biology and Endocrinology : RB&E·Chen XuXin Ni
Apr 16, 1999·Endocrine Reviews·L Aguilar-Bryan, J Bryan
May 29, 2003·British Journal of Pharmacology·Li-Ping HeLars Cleemann
Oct 27, 2004·British Journal of Pharmacology·Marianne Glavind-KristensenChristian Aalkjaer

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