A physiological correlate of disuse-induced sprouting at the neuromuscular junction.
Recent investigations have established that many of the normal properties of muscle fibres are maintained, at least in part, by muscle activity. Thus, a fall in resting membrane potential, an increase in input resistance, and spread of acetylcholine receptors to extrajunctional sites can all be induced by abolishing muscle activity and prevented by direct stimulation of denervated muscle fibres. Muscle activity also exerts a trophic influence on the innervating motoneurones; furthermore it may be a factor in the regulation of sprouting. Brown and Ironton found fine, "ultra-terminal sprouts" emanating from the endplates of muscles rendered inactive by chronic conduction block of the muscle nerve. Pestronk and Drachman saw increased branching of the motor nerve terminal and a consequent increase in endplate size in similar conditions. If these sprouts at the endplates of inactive muscles were functional, one might expect more transmitter to be released in response to nerve stimulation. We report here that both quantum content and spontaneous miniature endplate potential (m.e.p.p) frequency are increased at the terminals of inactive (disused) muscles.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D005260:Female; D008297:Male; D008564:Membrane Potentials; D009045:Motor Endplate / Q000502:physiology; D009121:Muscle Denervation; D009469:Neuromuscular Junction / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D009435:Synaptic Transmission; D013779:Tetrodotoxin / Q000494:pharmacology
D013779:Tetrodotoxin; D000109:Acetylcholine