Effect of myasthenic immunoglobulin on acetylcholine receptors of intact mammalian neuromuscular junctions.
Degradation of acetylcholine receptors of intact mouse neuromuscular junctions was determined in vivo and in vitro by the release of radioactivity from mouse diaphragms labeled with 125I-alpha-bungarotoxin. Treatment of mice with immunoglobulin from myasthenic patients accelerated the degradation rate to approximately three times normal, in both intact animals and organ cultures. The released radioactivity was in the form of [125I]tyrosine, confirming the nature of the degradative process. Accelerated degradation of acetylcholine receptors at neuromuscular junctions may represent an important antibody-mediated mechanisms in myasthenia gravis.
D000818:Animals; D000937:Antigen-Antibody Reactions; D001323:Autoantibodies; D002038:Bungarotoxins / Q000378:metabolism; D003964:Diaphragm; D006801:Humans; D051379:Mice; D009157:Myasthenia Gravis / Q000276:immunology* / Q000378:metabolism; D009469:Neuromuscular Junction / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000378:metabolism*
D001323:Autoantibodies; D002038:Bungarotoxins; D011950:Receptors, Cholinergic