Depolarization of the motor endplate region by decamethonium and acetylcholine / by B. Delisle Burns and W.D.M. Paton.

  • Burns, B. Delisle (Benedict Delisle)
Date:
[1951?]
Catalogue details

Licence: In copyright

Credit: Depolarization of the motor endplate region by decamethonium and acetylcholine / by B. Delisle Burns and W.D.M. Paton. Source: Wellcome Collection.

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    [Reprinted from the Journal of Physiology, 1951, Vol. 115, No. 1, p. 41.] PRINTED IN GREAT BRITAIN J. Physiol. (1951) 115, 41-73 DEPOLARIZATION OF THE MOTOR END-PLATE BY DECAMETHONIUM AND ACETYLCHOLINE By B. DELISLE BURNS and W. D. M. PATON From the National Institute for Medical Research, Mill Hill, London, N.W. 7 (Received 13 March 1951) Decamethonium was first investigated because, like D-tubocurarine, it caused neuromuscular block. It was shown, however, that the action of decamethonium was not only unlike that of curare but, in many important respects, was similar to that of acetylcholine (Paton & Zaimis, 1949; Buttle & Zaimis, 1949; Zaimis, 1951). For instance, both compounds elicit a twitch from cat muscle if injected into the artery, both cause contracture of frog’s rectus and of avian muscle, and both are antagonized by D-tubocurarine. Further, it has been found that decamethonium, like acetylcholine, depolarizes the muscle fibre; thus a dose of decamethonium, adequate to block neuromuscular transmission completely, reduced the injury potential of the cat’s tibialis muscle by 30-50% (Brown, Paton & Yianna Dias, 1949). Such a depolarization, affecting the whole length of every muscle fibre in the body, seemed likely to cause measurable changes in the distribution of sodium and potassium. With this in mind, the uptake of 24Na by muscles under the influence of decamethonium was investigated (J. L. Malcolm & W. D. M. Paton, unpublished). It was found, however, that the uptake of 24Na by frog sartorii from Ringer containing this isotope was not significantly greater in the presence of decamethonium iodide (0-01 %) than in its absence; further, the level of plasma 24Na in a cat which had received an injection of sodium chloride rich in this isotope, was altered by less than 1% when a massive dose of decamethonium was injected which caused long-lasting neuromuscular block. Whether or not the argument on which these experiments were based was justified, the results made us suspect that the depolarizing effect of the drug was not uniform throughout the length of the muscle fibre, but was restricted to the region of the end-plate. Most of the experiments described in this paper have been on the cat’s gracilis muscle, in which the end-plate region is conveniently localized. The results show that the depolarization due to decamethonium is confined to the membrane of the muscle fibre within 3-4 mm. of the end-plate. As a consequence of this local depolarization, electrical excitability around the end-plates falls,