Abstract
The development of experimental autoimmune myasthenia gravis (EAMG) was studied in 10 rabbits which were repeatedly injected with Torpedo acetylcholine receptor (AChR). Serum samples were obtained at various times for determination of complement fixing antibody level, serum complement level and the capacity of serum to inhibit neuromuscular transmission in amphibian muscle (passive transfer inhibiting capacity, PTIC). In seven animals the rise in level of circulating antibody occurred immediately before or in synchrony with the development of EAMG and frequently at such times serum complement rose irregularly. The PTIC was elevated during appearance of EAMG. In some animals a rise in complement fixing antibody level occurred without appearance of EAMG; in two others EAMG appeared without significant rise in antibody level. The data indicate that development of EAMG is associated with the production of antibodies which are capable of depressing neuromuscular transmission by reducing the sensitivity of the postjunctional membranes to acetylcholine. This depression can be potentiated by serum complement. Some but not all of the antibodies produced appear to fix complement when combined with Torpedo AChR. Evidence indicating possible existence of a presynaptic contribution to the development of EAMG is given.
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