Anti-acetylcholine receptor antibodies directed against the alpha-bungarotoxin binding site induce a unique form of experimental myasthenia.

Of seven rat monoclonal antibodies directed against nicotinic acetylcholine receptor, the three whose binding was blocked by alpha-bungarotoxin produced acute paralysis in chicken hatchlings, whereas the four others had no effect. In the affected animals, weakness and decremental electromyographic responses appeared within 1 hr after intravenous injection and both abnormalities improved after anticholinesterase administration. No histological changes were seen in the muscle of injected animals. These data suggest that antibodies binding in relationship to the cholinergic binding site, and presumably producing pharmacologic blockade of acetylcholine receptor, may play an important role in the pathogenesis of the defective neuromuscular transmission in myasthenia gravis.