Accelerated degradation of junctional acetylcholine receptor-alpha-bungarotoxin complexes in denervated rat diaphragm.
[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.
D000818:Animals; D002038:Bungarotoxins / Q000378:metabolism*; D003714:Denervation; D003964:Diaphragm / Q000378:metabolism* / Q000601:surgery; D007365:Intercellular Junctions / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011950:Receptors, Cholinergic / Q000378:metabolism*
D002038:Bungarotoxins; D011950:Receptors, Cholinergic