Comparison of α-bungarotoxin binding to skeletal muscles after inactivity or denervation

Abstract

DENERVATION of skeletal muscles causes a spread of acetyl-choline (ACh) sensitivity along muscle fibres, but it is not yet clear whether this results from muscle inactivity or from a loss of trophic influence of the nerve on the muscle¹. It has been suggested that inactivity is responsible for the phenomenon because the application of a cuff containing a local anaesthetic to a nerve blocked the conduction of the nerve impulses and caused the development of widespread sensitivity to ACh (ref. 2, but see ref. 3). The local anaesthetics used in that study, however, have since been shown to block axoplasmic transport in vitro^4,5 and in vivo⁶, as well as to induce neuronal degeneration⁷. Axoplasmic transport seems to be involved in the trophic influence of the nerve on muscle because blocking this transport induces spreading of ACh sensitivity in muscle fibres^8,9. We have used tetrodotoxin (TTX), incorporated into silicone cuffs placed around motor nerves, to test whether the resultant inactivity induced a spread of ACh sensitivity in skeletal muscle, as inferred from the binding of α-bungarotoxin (α-BuTX). TTX was chosen because it does not block axoplasmic transport in vitro⁵.