AJP - Endocrinology and Metabolism, Vol 243, Issue 1 31-E36, Copyright © 1982 by American Physiological Society
Acetylcholine receptor turnover in myasthenia gravis
S. H. Appel, J. C. Blosser, J. L. McManaman and T. Ashizawa
Humoral antibodies directed against the acetylcholine receptor are present
in most patients with myasthenia gravis. These antibodies accelerate
receptor degradation and thus cause a decrease in receptor level and
impaired neuromuscular transmission. The stimulus that triggers and
sustains the formation of the antibodies has not been identified, but it is
possible that the primary antigen may be located on the cell surface of
thymic lymphocytes. In some situations the clinical state in myasthenia
gravis does not correlate with the antibody titer, suggesting that other
factors also influence receptor amount and/or function of other potential
regulators that have been investigated. Calcium and agents that increase
cyclic AMP appear to increase the formation of the receptor and thus might
serve to mitigate the effects of the circulating antibodies. In contrast,
cholinergic agonists may cause a further decrease in receptor number,
providing an explanation of why myasthenic patients may become resistant to
therapy.
