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Thapsigargin-sensitive cationic current leads to membrane depolarization, calcium entry, and insulin secretion in rat pancreatic -cells

Departments of ¹Biophysics and ²Cell Biology, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City, Mexico

Submitted 23 February 2005 ; accepted in final form 2 April 2005

Glucose-induced insulin secretion by pancreatic -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 -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 plasma membrane, producing electrical activity and increasing [Ca²⁺]_i. The latter is prevented by nifedipine, indicating that Ca²⁺ enters the cell through L-type Ca²⁺ channels, which are activated by membrane depolarization. Thapsigargin also increased insulin secretion by increasing the percentage of cells secreting insulin and amplifying hormone secretion by individual -cells. Nifedipine blocked the increase completely in 5.6 mM glucose 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.

nonselective cationic channels; calcium channels; stimulus-secretion coupling

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