Chronic experimental autoimmune myasthenia gravis induced by monoclonal antibody to acetylcholine receptor: biochemical and electrophysiologic criteria.
To determine whether the chronic presence of antibody to acetylcholine receptor (AChR) can account for the neuromuscular abnormalities in myasthenia gravis (MG), rats injected repeatedly with monoclonal antibody (mAb) to AChR were compared with those injected with control mAb. In a previous report, those receiving anti-AChR mAb, studied ultrastructurally, had grossly simplified endplates when compared with normal controls. In this report, animals injected once or chronically for 9 to 12 wk had reduced content of muscle AChR. The chronically injected animals also had diminished miniature endplate potential amplitudes, but to a lesser extent than the reduction in AChR content. These studies establish the pathogenetic role of antibody to AChR in the induction of the ultrastructural, biochemical, and electrophysiologic hallmarks of MG.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D000918:Antibody Specificity; D004306:Dose-Response Relationship, Immunologic; D008564:Membrane Potentials; D009045:Motor Endplate / Q000503:physiopathology; D009132:Muscles / Q000503:physiopathology; D009157:Myasthenia Gravis / Q000276:immunology* / Q000503:physiopathology; D009469:Neuromuscular Junction / Q000503:physiopathology; D051381:Rats; D011978:Receptors, Nicotinic / Q000276:immunology*; D009435:Synaptic Transmission
D000911:Antibodies, Monoclonal; D011978:Receptors, Nicotinic