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AMPA Receptors Regulate Exocytosis and Insulin Release in Pancreatic β Cells
Author(s) -
Wu ZhenYong,
Zhu LiJun,
Zou Na,
Bombek Lidija K.,
Shao ChongYu,
Wang Na,
Wang XinXin,
Liang Li,
Xia Jun,
Rupnik Marjan,
Shen Ying
Publication year - 2012
Publication title -
traffic
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.677
H-Index - 130
eISSN - 1600-0854
pISSN - 1398-9219
DOI - 10.1111/j.1600-0854.2012.01373.x
Subject(s) - exocytosis , biology , ampa receptor , glutamate receptor , depolarization , microbiology and biotechnology , insulin , ionotropic effect , diazoxide , ionotropic glutamate receptor , receptor , biochemistry , secretion , endocrinology
Ionotropic glutamate receptors ( iGluRs ) are expressed in islets and insulinoma cells and involved in insulin secretion. However, the exact roles that iGluRs play in β cells remain unclear. Here, we demonstrated that GluR2 ‐containing α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptors ( AMPARs ) were expressed in mouse β cells. Glutamate application increased both cytosolic calcium and the number of docked insulin‐containing granules, which resulted in augmentation of depolarization‐induced exocytosis and high‐glucose‐stimulated insulin release. While glutamate application directly depolarized β cells, it also induced an enormous depolarization when K ATP channels were available. Glutamate application reduced the conductance of K ATP channels and increased voltage oscillations. Moreover, actions of AMPARs were absent in Kir 6.2 knock‐out mice. The effects of AMPARs on K ATP channels were mediated by cytosolic cGMP . Taken together, our experiments uncovered a novel mechanism by which AMPARs participate in insulin release.