DENERVATION of striated muscle leads to characteristic histological, histochemical, physiological, and pharmacological changes which have been ascribed to the loss of a trophic influence of nerve on muscle. The exact nature of this trophic effect has not been determined, although the release of acetylcholine at the motor end-plate seems necessary to maintain the relative insensitivity of normal muscle fibers to this substance away from the end-plate region.1,2 The observations of Miledi3,4 suggest that an influence other than acetylcholine is also important. Eccles5 has postulated the existence of a trophic substance which passes from nerve to muscle and is independent of neural activity.
Since denervation of muscle leads to a loss of muscle activity, and disuse of muscle without denervation can also lead to change,6,7 it seems necessary to consider the role of disuse alone in the pathogenesis of the denervation change.
It has been demonstrated
Brooks JE. Disuse Atrophy of Muscle: Intracellular Electromyography. Arch Neurol. 1970;22(1):27–30. doi:10.1001/archneur.1970.00480190031005
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