Abstract
D-TUBOCURARINE is one of the most widely used drugs in pharmacology, physiology and anaesthesia. It is generally assumed that the muscle paralysis produced by its administration is due to competition with acetylcholine (ACh), the nerve muscle transmitter, for receptor sites at the endplate1. There is no doubt that D-tubocurarine does act postsynaptically. But the question arises, is this its only action2? Special importance has been given to this question recently by the report3 that D-tubocurarine reduces the depolarizing action of iontophoretically applied ACh much less than it reduces the amplitude of the endplate potentials (e.p.p.s) produced by the depolarizing action of the natural transmitter, implying a possible presynaptic effect.
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HUBBARD, J., WILSON, D. & MIYAMOTO, M. Reduction of Transmitter Release by D-Tubocurarine. Nature 223, 531–533 (1969). https://doi.org/10.1038/223531a0
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DOI: https://doi.org/10.1038/223531a0
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