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The Ionic Basis of Inhibitory Presynaptic Modulation and Substance B a
Author(s) -
COOPER JACK R.,
ZOLTAY GABOR
Publication year - 1990
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1990.tb31985.x
Subject(s) - inhibitory postsynaptic potential , acetylcholine , veratridine , chemistry , biophysics , hyperpolarization (physics) , depolarization , substance p , muscarine , neuroscience , pharmacology , neuropeptide , stereochemistry , muscarinic acetylcholine receptor , biochemistry , receptor , biology , sodium , sodium channel , organic chemistry , nuclear magnetic resonance spectroscopy
We have investigated the possibility that, regardless of the involvement of a second messenger system, the ultimate effect of presynaptic, receptor-activated inhibitory modulation is the opening of a K channel. This possibility was explored utilizing rat cortical synaptosomes that were prelabeled with either 86Rb or [3H]acetylcholine, depolarizing with either K+ or veratridine, and measuring either efflux of 86Rb or release of [3H]acetylcholine in the presence or absence of inhibitory presynaptic modulators. The modulating agents used were 2-chloroadenosine, carbamylcholine, clonidine, and morphine. In all instances, these agents promoted an increased efflux of 86Rb, indicating hyperpolarization, and decreased release of acetylcholine. These results support our contention that an increase in K conductance may be responsible for presynaptic inhibition of the release of neurotransmitters. We have also found that substance B, a compound that reverses presynaptic modulation, appears to act by closing K channels.