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pubmed:abstractText |
Several factors, which prolonged the decay of the endplate current (EPC) without the loss of its exponential nature, were studied in voltage-clamp experiments on frogs. The ability of some factors to prolong EPC decay (acetylcholinesterase inhibition, ethanol) was reduced after acetylcholine receptors (AChR) density decreased upon treatment with alpha-bungarotoxin. The effect of other factors (hyperpolarization, cooling, "very fast" channel blocker dipyroxime) was independent of the AChR density. It was concluded that among mechanisms of EPC prolongation sensitive to the AChR' density, there are some connected with a decrease in the acetylcholinesterase activity and others altering the kinetics of AChR function.
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