Abstract
The present experiments investigated the release of [ 3H]acetylcholine ([ 3H]ACh) from the guinea pig myenteric plexus treated with 2-(4-phenylpiperidino)cyclohexanol (vesamicol), a drug that impairs ACh accumulation by synaptic vesicles. Ouabain, an Na +-K + ATPase inhibitor, released [ 3H]ACh synthesised in the presence of (−)-vesamicol, while electrical field stimulation or KCl depolarisation were not effective to release the transmitter in this condition. The effect of ouabain was Ca 2+-dependent and in the presence of (−)-vesamicol it was blocked by calphostin C, an inhibitor of protein kinase C (PKC). In addition, stimulation of kinase C activity by a phorbol ester, but not by its inactive isomer, prevented (−)-vesamicol from interfering with the release of [ 3H]ACh in electrically-stimulated myenteric plexus, similar to the effect of ouabain. We conclude that release of [ 3H]ACh induced by ouabain in the presence of (−)-vesamicol depends on PKC activation.
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