Pachter B R, Davidowitz J, Breinin G M
Am J Pathol. 1976 Jan;82(1):111-8.
The fine structure of end-plate abnormalities was studied in the Bar harbor C57Bl/6jdy2j dystrophic mouse. A marked increase in area and volume of junctional sarcoplasm was often apparent. Such hypertrophied end-plates were often penetrated by networks of axonal terminal branches. At times, pseudopod-like extensions of the junctional sarcoplasm encompassed and made protracted synaptic contact with the incoming axon. Such apparent remodeling of the neuromuscular apparatus might represent a compensatory cellular response to decreased impulse transmission efficiency, as might result from a flattening of the postjunctional folding seen on abnormal muscle fibers in these animals.
在巴尔港C57Bl/6jdy2j营养不良小鼠中研究了终板异常的精细结构。连接肌浆的面积和体积通常明显增加。这种肥大的终板常常被轴突终末分支网络穿透。有时,连接肌浆的伪足样延伸会包围传入轴突并与之进行长时间的突触接触。神经肌肉装置的这种明显重塑可能代表了对冲动传递效率降低的一种代偿性细胞反应,这可能是由于在这些动物的异常肌纤维上看到的突触后褶皱变平所致。