Role of axoplasmic transport in neurotrophic regulation of muscle end plate acetylcholinesterase.

Abstract

THE mechanism underlying neural control of skeletal muscle acetylcholinesterase (AChE) is not fully understood1. The experimental evidence points to acetylcholine (ACh)2 and nerve-evoked muscle activity3 as the “trophic” mediators, but neither is sufficient to account for the entire effect of innervation on muscle4. It remains to be seen whether factors such as cell-to-cell contact, and/or some regulatory substance(s) released by motor nerves also contribute to the regulation of AChE activity. In turn, the regulatory substance(s) might be conveyed by axoplasmic transport, for blockage of this process causes denervation-like changes without disturbing neurotransmitter release or the consequent muscle contractile activity5. We report here a reversible change in the activity of endplate AChE that can be ascribed to a temporary interruption of axoplasmic transport.