Abstract

Chickens with hereditary muscular dystrophy have been reported to have abnormalities in acetylcholinesterase (AChE) activity and therefore muscles of this genotype may not be able to respond to neural influences. We compared the trophic control of AChE activity in muscle cultured from dystrophic embryos with that from normal embryos. With standard culture media, no differences were noted in the development of AChE activity in muscle cultured from normal and dystrophic embryos. Addition of culture media containing a neural extract prepared by ammonium sulfate precipitation of sheep sciatic nerve consistently produced a significant increase in AChE activity in normal but not in dystrophic muscle. The data, in addition to showing that trophic activity is present in ammonium sulfate-precipitated fractions of sheep sciatic nerve, demonstrate an inability of muscle of the dystrophic genotype to respond to a neurotrophic influence. Under standard culture conditions, skeletal muscle of the dystrophic genotype has the capability to synthesize AChE, and therefore the failure to respond to a trophic influence may indicate the absence of a receptive mechanism for detecting the mediator(s) of the neurotrophic effect.

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