慢性实验性变应性猴脑脊髓炎的超微结构改变

来源 :中华神经科杂志 | 被引量 : 0次 | 上传用户:tourer
下载到本地 , 更方便阅读
声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架
论文部分内容阅读
目的 探讨自身免疫性中枢神经系统脱髓鞘疾病慢性型的病理特点及其可能机制。方法 成功建立猴实验性变态反应性脑脊髓炎模型数年后 ,根据MR摄片结果定位病灶并作分类 ,然后进行病理取材和电镜观察超微结构。结果  (1)活动性病灶内见成片的髓鞘松解、断裂或融合 ,轴突空泡样变性、皱缩或消失 ,少突胶质细胞变性 ,未见淋巴细胞浸润 ,仅见散在巨噬细胞 ,伴明显的间质水肿 ;(2 )可疑活动性病灶内见部分髓鞘内板松解 ,其内轴突有轻度空泡样变 ,亦见少突胶质细胞变性 ,散在巨噬细胞 ,未见淋巴细胞浸润。结论 慢性EAE的病理改变不仅有髓鞘的变性 ,同时轴突的病变也十分明显。 Objective To investigate the pathological features and possible mechanisms of chronic type of autoimmune demyelinating diseases of the central nervous system. Methods After successfully establishing monkey experimental allergic encephalomyelitis model for several years, the lesions were classified and classified according to the results of MR imaging. Then the ultrastructure was observed by pathology and electron microscopy. Results (1) In the active lesion see the piece of myelin loose, fracture or fusion, axonal vacuolar degeneration, shrinkage or disappearance of oligodendrocyte degeneration, no lymphocyte infiltration, only see scattered macrophages Cells, with obvious interstitial edema; (2) suspicious activity of the lesion see part of the myelin inner plate loosening, there is a slight vacuolar degeneration of the axons, also see degeneration of oligodendrocytes, scattered macrophages Cells, no lymphocytic infiltration. Conclusion The pathological changes of chronic EAE not only demyelination, axonal lesions are also very obvious.
其他文献
目的 探讨海马 μ型阿片受体 (MORs)在红藻氨酸 (KA)诱导的癫痫敏感性形成机制中的作用。方法 惊厥剂量KA(10mg/kg)皮下注射诱导大鼠癫痫发作 ,应用微渗透泵技术在大鼠腹侧