Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:383-387 Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis II. Receptor synthesis

SUMMARY The in vivo synthesis of diaphragm endplate acetycholine receptors was estimated in mice treated daily with IgG from eight myasthenia gravis patients.- Myasthenia gravis IgG prep-arations which had previously been shown to increase the rate of receptor degradation also increased the rate of receptor synthesis, suggesting the existence of a compensatory mechanism serving to stabilise the number of acetycholine receptors. An increased rate of acetylcholine receptor (AChR) degradation is thought to play an important role in the loss of end-plate AChRs which occurs in myas-thenia gravis (MG). The rate of loss of 125I-a-bungarotoxin (a-butx)-labelled AChRs is increased both in myoblast cultures12 and in mice injected daily with IgG prepared from MG patients.3 We have confirmed these results but find that the increased rate of degradation is not an invariable result of human antibodies binding to mouse AChR at the end-plate.4 Moreover, even in those animals in which an increased rate of AChR degradation could be demonstrated the total number of acetyl-choline receptors present at the end-plate after seven daily IgG injections was reduced less than predicted from the increased degradation rate. These observations suggested that an increased rate of AChR synthesis might compensate for the increased rate of degradation that occurred with some IgG preparations4 and in this paper we describe the results of experiments designed to test this possibility. End-plate AChRs were first blocked by intrathoracic injection of non-radioactive a-butx. The animals then received daily injections of IgG. The rate of synthesis of new AChRs, free from a-butx, was measured at various time intervals by removing the diaphragms and incubating in radioac-tive a-butx in vitro. AChR synthesis was increase