Rbbits were immunized with purified acetylcholine receptor from Narke electroplax japonica. A defect of neuromuscular transmission, physiologically identical to human myasthenia gravis, developed when antibodies against the receptor were found in serum. To clarify the mode of action of these antibodies, changes in the endplate current of frog muscle fibers were recorded after exposure to immune rabbit sera. The rabbit sera depressed the amplitude of the endplate current, but caused no change in the time course or the dependence of amplitude and half-decay time on membrane potential. Antibodies may affect acetylcholine binding without impairing ionophore function.