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4‐Aminopyridine interrupts the modulation of acetylcholine release mediated by muscarinic and opiate receptors
Author(s) -
Törőcsik A.,
Vizi E. S.
Publication year - 1990
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490270213
Subject(s) - chemistry , oxotremorine , muscarinic acetylcholine receptor , 4 aminopyridine , acetylcholine , physostigmine , agonist , muscarinic acetylcholine receptor m2 , pharmacology , endocrinology , muscarinic agonist , medicine , biophysics , potassium channel , receptor , biochemistry , biology
Abstract The effect of 4‐aminopyridine, a potassium channel blocker on the muscarinic and opiate modulation of acetylcholine release, was investigated. Rat frontal cortical slices were loaded with [ 3 H]choline, super‐fused continuously, and stimulated electrically. 4‐Aminopyridine enhanced the stimulation‐evoked release of tritium without affecting basal release. The electrically evoked release of radioactivity was reduced by the muscarinic agonist oxotremorine and the delta selective opiate receptor agonist Metenkephalin, and was enhanced—in the presence of the cholinesterase inhibitor physostigmine—by the muscarinic antagonist atropine. These effects were completely abolished by 4‐aminopyridine. Since 4‐aminopyridine blocks potassium permeability of the neuron, it is suggested that the changes in potassium permeability and the consequent alteration of membrane polarization are involved in the presynaptic modulation of acetylcholine release.