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From the First Department of Internal Medicine, Nagasaki University School of Medicine, and the Institute for Protein Research, Osaka University.
Neuromuscular transmission was studied electrophysiologically in rabbits intoxicated by
-bungarotoxin, a specific inhibitor of acetylcholine receptor. The findings consisted of a slight reduction in amplitude of single evoked muscle action potential, 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.
Requests for reprints should be addressed to Dr. Takamori, First Department of Internal Medicine, Nagasaki University School of Medicine, 7-1, Sakamoto-machi, Nagasaki, Japan.
This investigation was supported in part by the Myasthenia Gravis Research Grant funded by the Japanese Ministry of Health and Welfare (Dr. Takamori).
Received for publication October 27, 1975.
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