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.
D000109:Acetylcholine / Q000378:metabolism*; D000634:Aminoquinolines / Q000494:pharmacology; D000818:Animals; D001906:Botulism / Q000503:physiopathology; D008564:Membrane Potentials; D008959:Models, Neurological; D009045:Motor Endplate / Q000187:drug effects / Q000503:physiopathology; D009416:Nerve Regeneration; D009468:Neuromuscular Diseases / Q000503:physiopathology*; D009469:Neuromuscular Junction / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission
D000634:Aminoquinolines; C001920:4-aminoquinoline; D000109:Acetylcholine