PT  - JOURNAL ARTICLE
AU  - S. C. Taylor
AU  - E. Carpenter
AU  - M. L. Roberts
AU  - C. Peers
TI  - Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca<sup>2+</sup> Sensitivity of Exocytosis
AID  - 10.1523/JNEUROSCI.19-14-05741.1999
DP  - 1999 Jul 15
TA  - The Journal of Neuroscience
PG  - 5741--5749
VI  - 19
IP  - 14
4099  - http://www.jneurosci.org/content/19/14/5741.short
4100  - http://www.jneurosci.org/content/19/14/5741.full
SO  - J. Neurosci.1999 Jul 15; 19
AB  - 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.