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Physostigmine and neuromuscular transmission.
Ann N Y Acad Sci
June 1993
Laboratory of Molecular Neurobiology, Johannes-Gutenberg-University Medical School, Mainz, Germany.
Single channel studies carried out in cultured rat myoballs and cultured hippocampal neurons, and ion flux studies performed on Torpedo electrocyte membrane vesicles, showed that physostigmine (Phy), a well-established acetylcholinesterase inhibitor, interacts directly with nicotinic acetylcholine receptors (nAChR). Low concentrations (0.1 microM) of Phy activate the receptor integral channel, whereas higher concentrations blocked the channel in its opened state.
View Article and Find Full Text PDFA second pathway of activation of the Torpedo acetylcholine receptor channel.
Eur J Biochem
September 1991
Institute of Physiological Chemistry, Johannes-Gutenberg University Medical School, Mainz, Federal Republic of Germany.
We have studied the interaction of the reversible acetylcholine esterase inhibitor (-)physostigmine (D-eserine) with the nicotinic acetylcholine receptor (nAChR) from Torpedo marmorata electric tissue by means of ligand-induced ion flux into nAChR-rich membrane vesicles and of equilibrium binding. We find that (-) physostigmine induces cation flux (and also binds to the receptor) even in the presence of saturating concentrations of antagonists of acetylcholine, such as D-tubocurarine, alpha-bungarotoxin or antibody WF6. The direct action on the acetylcholine receptor is not affected by removal of the methylcarbamate function from the drug and thus is not due to carbamylation of the receptor.
View Article and Find Full Text PDFThe interaction of benzoquinonium and other neuromuscular blocking agents.
Acta Pharmacol Toxicol (Copenh)
July 2000
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