Presynaptic function modified by acetylcholine-receptor interaction in experimental autoimmune myasthenia gravis.

Rats with experimental autoimmune myasthenia gravis (EAMG) were studied to test if the postsynaptic receptor disease would be modified by a compensating presynaptic effect of acetylcholine (ACh) being mediated through the presynaptic receptor. In normal rat phrenic-diaphragms, the ACh quantum content was estimated using the cut-muscle technique by which the evoked release of transmitter can be measured in the absence of blocking agents; values were significantly increased when the ACh receptor was blocked by d-tubocurarine. In rats with EAMG, this presynaptic autoregulation acted to compensate the postsynaptic failure, but did not reach the range of d-tubocurarine-treated controls. Results may be explained by either the difference between the receptor sites for myasthenic antibodies and d-tubocurarine or the immunological property of the presynaptic receptor which may differ from the postsynaptic one.