Colloque

Neuro-anatomical site in tick paralysis

Maurice F. Murnaghan

Membre a labase

Maurice F. Murnaghan

Résumé du colloque

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 not appear to be the underlying mechanism because choline acetylase activity in the anterior motor roots and peroneal nerve is normal and large doses of acetylcoenzyme A do not influence the paralysis. Failure of acetylcholine liberation appears to be restricted to the terminals of somatic motor nerves because autonomic ganglionic transmission persists in the paralysed animal.