Sodium channels contribute to action potential generation in canine and human pancreatic islet B cells |
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Authors: | David M. Pressel Stanley Misler |
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Affiliation: | (1) Departments of Medicine (Jewish Hospital) and Cell Biology/Physiology, Washington University, 63110 St. Louis, Missouri;(2) Program in Neural Sciences, Washington University, 63110 St. Louis, Missouri |
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Abstract: | Summary Pancreatic islet B cells depolarize and display trains of action potentials in response to stimulatory concentrations of glucose. Based on data from rodent islets these action potentials are considered to be predominantly Ca2+ dependent. Here we describe Na+-dependent action potentials and Na+ currents recorded from canine and human pancreatic islet B cells. Current-clamp recording using the nystatin perforated-patch technique demonstrates that B cells from both species display tetrodotoxin-sensitive Na+ action potentials in response to modest glucose-induced depolarization. In companion whole-cell voltage-clamp experiments on canine B cells, the underlying Na+ current displays steep voltage-dependent activation and inactivation over the range of –50 to –40 mV. The Na+ current is sensitive to tetrodotoxin block with aK1=3.2nm and has a reversal potential which changes with [Na+]o as predicted by the Nernst equation. These results suggest that a voltage-dependent Na+ current may contribute significantly to action potential generation in some species outside the rodent family. |
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Keywords: | Na+ channels action potentials pancreatic islet B cell islet cell electrophysiology |
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