Abstract
In bullfrog sympathetic ganglion cells, muscarine produced an inward current ( I mus) through the activation of a subtype (M 1) of muscarinic acetylcholine receptor (mAChR) by suppressing an outward M-current ( I M), and/or activating cation-selective current ( I D; see below). The former was induced with a potency ( K d = 0.5 μM) higher than the latter ( K d = 5 μM) before and after blocking a fraction of the receptor with an irreversible blocker. Activators of protein kinase C mimicked muscarine's actions. Blocking I M by Ba 2+ increased I D. These results suggest that activation of M 1-mAChR both closes M-channel and opens cation-selective D-channel through phosphoinositide breakdown and the subsequent activation of protein kinase C and that a difference in potency at the last step of the cascade determines the order in which channels are regulated.
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