Experimental myasthenia due to alpha-bungarotoxin.

Neuromuscular transmission was studied electrophysiologically in rabbits intoxicated by alpha-bungarotoxin, a specific inhibitor of acetylcholine receptor. The findings consisted of a slight reduction in amplitude of single evoked muscle action potentials, a decrement in amplitude of successive evoked muscle action potentials post-tetanic potentiation and exhaustion, edrophonium reversal, and no change of muscle action potentials evoked by direct stimulation of the muscle. These were similar to characteristic electrophysiologic phenomena seen in 40 patients with myasthenia gravis. The receptor abnormality may be responsible for the underlying defect of myasthenia.