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Am J Physiol Endocrinol Metab (April 5, 2005). doi:10.1152/ajpendo.00082.2005
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Submitted on February 23, 2005
Accepted on April 2, 2005

A THAPSIGARGIN-SENSITIVE CATIONIC CURRENT LEADS TO MEMBRANE DEPOLARIZATION, CALCIUM ENTRY AND INSULIN SECRETION IN RAT PANCREATIC BETA-CELLS

R. Cruz-Cruz1, A. Salgado1, C. Sanchez-Soto1, L. Vaca1, and M. Hiriart1*

1 Department of Biophysics, Inst Fisiol Cel UNAM, Mexico, DF, Mexico

* To whom correspondence should be addressed. E-mail: mhiriart{at}ifc.unam.mx.

Glucose-induced insulin secretion by pancreatic {beta}-cells depends on membrane depolarization and [Ca2+]i increase. We correlated voltage- and current-clamp recordings, [Ca2+]i measurements and insulin reverse hemolytic plaque assay to analyze the activity of a thapsigargin-sensitive cationic channel that can be important for membrane depolarization in single rat pancreatic {beta}-cells. We demonstrate the presence of a thapsigargin-sensitive cationic current which is mainly carried by Na+. Moreover, in basal glucose concentration (5.6 mM), thapsigargin depolarizes the plasmatic membrane producing electrical activity and increases [Ca2+]i. The later is prevented by nifedipine, indicating that Ca2+ enters the cell through L-type Ca2+ channels that are activated by membrane depolarization. Thapsigargin also increased insulin secretion by raising the percentage of cells secreting insulin and amplifying hormone secretion by individual {beta}-cells. Nifedipine blocked this increase completely in 5.6 mM, and partially in 15.6 mM glucose. We conclude that thapsigargin potentiates a cationic current that depolarizes the cell membrane. This in turn, increases Ca2+ entry through L-type Ca2+-channels promoting insulin secretion.




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