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The Journal of Neuroscience, July 15, 1999, 19(14):5741-5749

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca²⁺ Sensitivity of Exocytosis

S. C. Taylor¹, E. Carpenter¹, M. L. Roberts², and C. Peers¹

¹ Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, United Kingdom, and ² Department of Physiology, University of Adelaide, Adelaide 5005, Australia

Electrochemical detection of quantal catecholamine release from PC-12 cells revealed that glibenclamide, an inhibitor of ATP-sensitive K⁺ channels, potentiated Ca²⁺-dependent exocytosis evoked by raised extracellular [K⁺] and by exposure of cells to caffeine. Glibenclamide was without effect on voltage-gated Ca²⁺ currents, membrane potential, or rises of [Ca²⁺]_i evoked by either raised extracellular [K⁺] or caffeine. The dependence of K⁺-evoked secretion on extracellular Ca²⁺ was shifted leftward in the presence of glibenclamide, with a small increase in the plateau level of release, suggesting that glibenclamide primarily increased the Ca²⁺ sensitivity of the exocytotic apparatus. Enhancement of secretion by glibenclamide was reversed by pinacidil and cromakalim, indicating that the effects of glibenclamide were mediated via an action on a sulfonylurea receptor. These results demonstrate that sulfonylurea receptors can modulate Ca²⁺-dependent exocytosis via a mechanism downstream of Ca²⁺ influx or mobilization.

Key words: glibenclamide; sulfonylurea; catecholamines; exocytosis; Ca²⁺; amperometry; K_ATP channel; pheochromocytoma

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19145741-09$05.00/0

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