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Spontaneous transmitter release in experimental neuromuscular disorders of the rat.

Examination of spontaneous miniature end-plate potentials (mepps) in rat skeletal muscle has revealed that in conditions such as botulinum poisoning, during nerve terminal regeneration or in the presence of the drug 4-aminoquinoline two types of acetylcholine release are responsible for the mepps. In addition to the mepps that correspond to the quantal component of a nerve impulse evoked end-plate potential, a second type of acetylcholine release occurs. The latter type of transmitter release gives rise to mepps with a more prolonged time to peak and frequently a larger than normal amplitude. It is unaffected by nerve terminal depolarization, transmembrane calcium fluxes, and other procedures known to enhance mepp frequency. In botulinum-poisoned muscles this secretory type of transmitter release dominates, being exclusively present in muscles where nerve stimulation fails to release transmitter. In normal muscle such a release is induced by 4-aminoquinoline, which may cause up to 50% of all the spontaneous mepps to be of that kind. It is suggested that the described secretion of acetylcholine serves a neurotrophic function.