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Opiates Inhibit Acetylcholine Release from Torpedo Nerve Terminals by Blocking Ca 2+ Influx
Author(s) -
Michaelson D. M.,
McDowall G.,
Sarne Y.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12779.x
Subject(s) - acetylcholine , torpedo , depolarization , (+) naloxone , chemistry , morphine , opiate , biophysics , ionophore , channel blocker , antagonist , pharmacology , acetylcholine receptor , calcium , receptor , biochemistry , biology , organic chemistry
In the present communication we report that Ca 2+ ‐dependent acetylcholine release from K + ‐depolarized Torpedo electric organ synaptosomes is inhibited by morphine, and that this effect is blocked by the opiate antagonist naloxone. This finding suggests that the purely cholinergic Torpedo electric organ neurons contain pre‐synaptic opiate receptors whose activation inhibits acetylcholine release. The mechanisms underlying this opiate inhibition were investigated by comparing the effects of morphine on acetylcholine release induced by K + depolarization and by the Ca 2+ ionophore A23187 and by examining the effect of morphine on 45 Ca 2+ influx into Torpedo nerve terminals. These experiments revealed that morphine inhibits 45 Ca 2+ influx into K + ‐depolarized Torpedo synaptosomes and that this effect is blocked by naloxone. The effects of morphine on K + depolarization‐mediated 45 Ca 2+ influx and on acetylcholine release have similar dose dependencies (half‐maximal inhibition at 0.5–1 μ M ), suggesting that opiate inhibition of release is due to blockage of the presynaptic voltage‐dependent Ca 2+ channel. This conclusion is supported by the finding that morphine does not inhibit acetylcholine release when the Ca 2+ channel is bypassed by introducing Ca 2+ into the Torpedo nerve terminals via the Ca 2+ ionophore.