Effects of epinephrine, ouabain, and insulin in experimental autoimmune myasthenia gravis.
To gain a clue to the target of anti-AChR antibody, rats with acute and chronic experimental autoimmune myasthenia gravis (EAMG) that was induced by immunization with Narke anti-acetylcholine receptor (AChR) were studied using agents acting on active Na-k transport. Postsynaptic response to epinephrine was defective in chronic EAMG with high titers of antibody, suggesting that active Na-K transport system modulated by cyclic adenosine monophosphate (AMP) may be affected primarily by antibody. Sensitivity to ouabain was less than normal in acute EAMG and became close to normal when treated with anticomplementary factor. Findings suggest that acute EAMG is a case of functional denervation. Normal response to insulin occurred in all phases of EAMG.
D000818:Animals; D001323:Autoantibodies / Q000378:metabolism; D001327:Autoimmune Diseases / Q000378:metabolism*; D001693:Biological Transport, Active / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology*; D005260:Female; D007328:Insulin / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009157:Myasthenia Gravis / Q000378:metabolism*; D009469:Neuromuscular Junction / Q000187:drug effects; D010042:Ouabain / Q000494:pharmacology*; D011188:Potassium; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects*; D012964:Sodium; D009435:Synaptic Transmission / Q000187:drug effects
D001323:Autoantibodies; D007328:Insulin; D011950:Receptors, Cholinergic; D010042:Ouabain; D012964:Sodium; D011188:Potassium; D004837:Epinephrine