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NEUROLOGY 1986;36:942
© 1986 American Academy of Neurology

Presynaptic modification of neuromuscular transmission by antiacetylcholine receptor antibody

Myasthenic serum and monoclonal antibody produced by transformed lymphocytes

Masaharu Takamori, MD, Sei'ichi Okumura, MD and Atsuko Yasuda, MD

Department of Neurology, Kanazawa University School of Medicine, Kanazawa, Japan.

When myasthenic serum or a monoclonal antiacetylcholine receptor (anti-AChR) antibody produced by human transformed lymphocytes and transferable to an animal was applied to rat diaphragms in vitro, presynaptic facilitation was demonstrated by changes in ACh quantal content of endplate potentials. The results correlated with ability of the antibody to block binding of {alpha}-bungarotoxin to AChR, but not with titers of anti-AChR antibody by immunoprecipitation assay and AChR degradation rate. Antibody to the receptor site near the ACh-binding site may act presynaptically to compensate for the postsynaptic failure in myasthenia gravis.

Address correspondence and reprint requests to Dr. Takamori, Department of Neurology, Kanazawa University School of Medicine, 13-1, Takara-machi, Kanazawa, Japan 920.

Supported in part by grants from Neuroimmunological Disorders Research Committee and NCNMMD (84), Japanese Ministry of Health and Welfare, and Tokyo Biochemical Research Foundation.

Accepted for publication November 6, 1985.






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