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August 1967

Is Acetylcholine the Trophic Neuromuscular Transmitter?

Author Affiliations

From the Laboratory of Neuroembryology, Department of Neurology, Tufts-New England Medical Center, Boston.

Arch Neurol. 1967;17(2):206-218. doi:10.1001/archneur.1967.00470260096011

THE IMMEDIATE effect of denervation of skeletal muscle is motor paralysis. Over the longer term, denervation leads to a series of alterations in the morphology, physiology, and metabolism of muscle which have been termed "atrophic."1,2 It is clear that the motor nerves alone supply the "trophic influence" which is capable of preventing these changes, while the sensory and sympathetic innervation play no significant role.3-5 The question of how the nerves exert this effect remains of paramount importance.

The weight of present evidence suggests that neither conduction of motor nerve impulses nor mechanical work of muscle are the factors necessary to prevent denervation atrophy of skeletal muscle. Elimination of conducted nerve impulses by various experimental techniques6-8 fails to reproduce fully the effects of denervation, provided that the motor nerves remain anatomically and functionally connected to the muscle. Furthermore, relieving skeletal muscle of its work load (for example,

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