Takamori M, Sakato S, Okumura S
J Neurol Sci. 1984 Nov-Dec;66(2-3):245-53. doi: 10.1016/0022-510x(84)90013-3.
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.
对患有实验性自身免疫性重症肌无力（EAMG）的大鼠进行研究，以测试突触后受体疾病是否会因乙酰胆碱（ACh）通过突触前受体介导的补偿性突触前效应而改变。在正常大鼠膈神经 - 膈肌标本中，采用切断肌肉技术估计ACh量子含量，通过该技术可在无阻断剂的情况下测量递质的诱发释放；当ACh受体被d - 筒箭毒碱阻断时，该值显著增加。在患有EAMG的大鼠中，这种突触前自身调节作用可补偿突触后功能衰竭，但未达到d - 筒箭毒碱处理对照组的范围。结果可能是由于重症肌无力抗体与d - 筒箭毒碱的受体位点不同，或者突触前受体的免疫特性可能与突触后受体不同所致。
