Muscular dystrophy in the mouse: neuromuscular transmission and the concept of functional denervation.

Abstract

The results of recent investigations by ourselves and others indicate that no form of denervation exists to any remarkable degree in dystrophic mouse skeletal muscles. This conclusion is based on the following information: Dystrophic nerve terminals liberate normal amounts of transmitter both spontaneously and during impulse-mediated activity. The characteristics of the release process, the size of the available store of transmitter, and the probability of release of transmitter in response to the invasion of an action potential appear to be normal. The sensitivity of the postsynaptic membrane to the transmitter is normal. Action potential generation in response to both direct and indirect excitation is normal. There is no unequivocal pharmacologic evidence of denervation in dystrophic skeletal muscle, even though dystrophic muscle fibers respond to surgical denervation in a normal fashion. Nerve terminal sprouting is extensive, but there is no evidence of collateral reinnervation.