Accelerated degradation of junctional acetylcholine receptor-alpha-bungarotoxin complexes in denervated rat diaphragm

Abstract

[125] alpha-bungarotoxin was administered to rats in vivo to label acetylcholine receptor in innervated diaphragm, 5-day denervated diaphragm, or diaphragm which had been denervated immediately before labeling. The rate of degradation of junctional toxin-receptor complexes was followed by sacrificing animals at various times after labeling. The rate of degradation of junctional toxin-receptor complexes was significantly faster in 5-day denervated left hemidiaphragm (t 1/2=2.0 days) than in innervated left hemidiaphragm (t 1/2=10.7 days). The rate of degradation of junctional toxin-receptor complexes in left hemidiaphragm denervated at the time of labeling was essentially identical to that in innervated muscle for 3 days but then increased to a significantly more rapid rate (t 1/2=3.7 days in the period 3.13 days after denervation and labelling). These findings support the concept that continuous innervation is needed to maintain the metabolic stability of junctional acetylcholine receptors.