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.
D000109:Acetylcholine / Q000378:metabolism*; D002038:Bungarotoxins / Q000378:metabolism*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007366:Intercostal Muscles / Q000294:innervation; D008297:Male; D009045:Motor Endplate / Q000378:metabolism; D009157:Myasthenia Gravis / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000378:metabolism*; D014403:Tubocurarine / Q000494:pharmacology
D002038:Bungarotoxins; D011950:Receptors, Cholinergic; D000109:Acetylcholine; D014403:Tubocurarine