Acetylcholine receptor in myasthenia gravis: increased affinity for alpha-bungarotoxin.

Studies of the binding of 125 I-labeled alpha-bungarotoxin to myasthenic motor end-plates have been interpreted as showing a decrease in the number of acetylcholine (ACh) receptors at these end-plates. Equilibrium binding studies of 125 I-tagged alpha-bungarotoxin rather than to a decreased number of receoptors. Our results show increased rather than decreased affinity of myasthenic receptors for alpha-bungarotoxin and also suggest that the number of ACh receptors is indeed reduced. The presence of a change in binding affinity, in addition to the reduced number of ACh receptors, suggests the presence of membrane changes that may contribute to the pathogenesis of myasthenia gravis.