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In anti-esterase treated muscle, repeated nerve impulses give rise to a cumulative depolarization of the endplate which persists for several seconds after the end of the tetanus. It has been suggested that this phenomenon may be due to a side-effect of the esterase inhibitors, namely a stabilization of opened ionic channels in the endplate membrane persisting after the transmitter has diffused away, rather than - as previously supposed - to an accumulated residue of acetylcholine which continues to act during the slow depolarization. The question has been studied by intracellular recording of endplate potential and current, in glycerol-pretreated frog sartorius muscle. Noise analysis has been used to distinguish between the alternative explanations. The results show that the post-tetanic depolarization of anti-esterase treated endplates is accompanied by membrane fluctuations which resemble typical ‘acetylcholine noise’, in size and time characteristics. It is concluded that at least a large part of the prolonged depolarization arises from continued action of a residue of acetylcholine which has accumulated during the tetanus and disappears slowly thereafter.
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Katz et al. (1975) studied this question.
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