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Muscarinic receptor modulation of glucose‐induced electrical activity in mouse pancreatic B‐cells
Author(s) -
Santos Rosa M.,
Rojas Eduardo
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80669-6
Subject(s) - muscarinic acetylcholine receptor , muscarinic acetylcholine receptor m1 , chemistry , modulation (music) , endocrinology , muscarinic acetylcholine receptor m3 , medicine , receptor , microbiology and biotechnology , biology , biochemistry , physics , acoustics
Acetylcholine (1–10 μM) depolarized the membrane and stimulated glucose‐induced bursts of electrical activity in mouse pancreatic B‐cells. The acetylcholine effects were mimicked by muscarine while nicotine had no effect on membrane potential. Pirenzepine, an antagonist of the classical M1‐type muscarinic receptors, but not gallamine (1–100 μM), an antagonist of the classical M2‐type receptors, antagonized the acetylcholine action on glucose‐induced electrical activity (IC 50 = 0.25 μM). Bethanechol, an agonist of the classical M2‐type muscarinic receptors, was approximately 100 times less effective than acetylcholine in stimulating the electrical activity. In addition, acetylcholine (1 μM) induced a marked increase (25%) in input resistance to the B‐cell membrane. The results indicate that acetylcholine exerted its effects on the B‐cell membrane by inhibiting K + conductance via activation of a muscarinic receptor subtype distinct from the classical M2‐type receptor.