Role of protein kinase C in the release of [ 3H]acetylcholine from myenteric plexus treated with vesamicol

• Published in: Neuroscience letters Vol. 244; no. 2; pp. 115 - 117
• Main Authors: Clarizia, A.D, Romano-Silva, M.A, Prado, V.F, Gomez, M.V, Prado, M.A.M
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 13.03.1998; Elsevier
• Subjects: Acetylcholine - metabolism; Acetylcholine release; Animals; Biological and medical sciences; Calcium - metabolism; Electric Stimulation; Enzyme Inhibitors - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Kinetics; Male; Myenteric Plexus - drug effects; Myenteric Plexus - physiology; Naphthalenes - pharmacology; Neuromuscular Depolarizing Agents - pharmacology; Ouabain; Ouabain - pharmacology; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Piperidines - pharmacology; Potassium Chloride - pharmacology; Protein kinase C; Protein Kinase C - metabolism; Synaptic vesicles; Synaptic Vesicles - drug effects; Synaptic Vesicles - physiology; Tritium; Vertebrates: nervous system and sense organs; Vesamicol; Vesicular acetylcholine transporter; Vesamicol; Synaptic vesicles; Protein kinase C; Acetylcholine release; Vesicular acetylcholine transporter; Ouabain; Enzyme; Transferases; Rodentia; Synaptic vesicle; Enteric nervous system; Vertebrata; Mammalia; Guinea pig; Neurotransmitter; Acetylcholine; Myenteric plexus; Release
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(98)00143-8

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.