Plasma from myasthenia gravis patients reduces acetylcholine receptor agonist-induced Na flux into TE671 cell line

Plasma from myasthenia gravis patients was tested for its ability to inhibit agonist-induced 22Na+ influx into the TE671 cell line that expresses human acetylcholine receptors. Reduced 22Na+ influx correlated weakly with the total anti-acetylcholine receptor antibody level in the plasma, and was also related to the presence of antibody directed against the agonist binding site, as detected by inhibition of 125I-alpha-bungarotoxin binding. However, in some cases there was inhibition of 22Na+ flux without evident anti-alpha-bungarotoxin binding site antibody. We conclude that in most patients antibodies that interfere with 22Na+ influx do so by blocking the agonist binding site. However, in some cases antibodies may be directed at the Na+ ion channel or some important functional determinant.