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Previous work by the author suggested that the paralysis produced experimentally in dogs was probably due to failure in the liberation of acetylcholine at the neuro-muscular junction. This hypothesis was further substantiated by later findings that the paralysed muscle not only contracts on close intra-arterial injection of acetylcholine but is also more sensitive, being similar to a denervated one, and that neither action nor end-plate potentials could be detected during nerve stimulation. Recently it has been demonstrated that acetylcholine is not liberated by the perfused paralysed muscle when stimulated either directly or indirectly. Interference in the synthesis of acetylcholine does …
