Arizono N, Takeoka O, Hasegawa M, Yonezawa T, Yamaguchi K
Acta Pathol Jpn. 1985 May;35(3):621-9. doi: 10.1111/j.1440-1827.1985.tb00603.x.
Experimental autoimmune myasthenia gravis (EAMG) was produced in rabbits by the injection of acetylcholine receptor (AChR) protein from electric organ of Narkacion tokyonis with complete Freund's adjuvant, and the ultrastructural alterations of the neuromuscular junctions were studied. A lesion comparable to human myasthenia gravis could be observed in these animals. In acute EAMG, which showed a rapidly progressive severe paralysis 19 to 24 days after the first inoculation, distinct degeneration of the postsynaptic membrane was observed. Sometimes an irregular gap was found between the nerve terminal and postsynaptic sarcoplasm. In chronic EAMG with mild and prolonged muscle weakness, which appeared 23 to 54 days after the first inoculation, poorly developed junctional folds with little degenerative change were seen. By a morphometric analysis, some of the changes were detected even in a subclinical EAMG. In the presynaptic region, there was no ultrastructural alteration except that an increase of nerve terminal area was observed in chronic and subclinical EAMG. The pathogenesis of these alterations was discussed.
通过将来自东京电鳐电器官的乙酰胆碱受体(AChR)蛋白与完全弗氏佐剂一起注射到兔子体内,制备实验性自身免疫性重症肌无力(EAMG),并研究神经肌肉接头的超微结构改变。在这些动物中可观察到与人类重症肌无力相当的病变。在急性EAMG中,首次接种后19至24天出现快速进展的严重麻痹,观察到突触后膜明显变性。有时在神经末梢和突触后肌浆之间发现不规则间隙。在首次接种后23至54天出现的伴有轻度和持续性肌无力的慢性EAMG中,可见发育不良的突触褶皱且几乎没有变性改变。通过形态计量分析,即使在亚临床EAMG中也检测到了一些变化。在突触前区域,除了在慢性和亚临床EAMG中观察到神经末梢面积增加外,没有超微结构改变。讨论了这些改变的发病机制。