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目的 观察丙烯酰胺 (ACR)中毒后变异的C5 7BL/Ola(Ola)鼠与正常的C5 7BL/ 6J(6J)鼠轴突逆行性坏死的病理改变及两种鼠的不同点 ;探讨轴突与神经元损伤的关系。方法 利用光镜和电镜技术对腓神经、腓肠神经及背根神经节神经元的改变进行定性和定量分析。结果 光镜下 6J鼠总纤维面积明显增大 ,纤维密度明显降低 ,大径纤维减少 ;轴突肿胀 ,髓鞘深染 ,形状不规则。背根神经节中一些亮细胞 (A型细胞 )核偏向一侧 ,胞浆内有一些暗颗粒。电镜下见轴突内神经微丝增多 ,线粒体堆积。背根神经节细胞胞浆内线粒体呈空泡样或凝聚样变性。Ola鼠未见明显改变。结论 Ola鼠对ACR所致的类华勒氏变性反应是延迟的 ,而 6J鼠中毒后出现轴突肿胀、变性 ,电镜下以神经微丝的聚集、线粒体堆积为特征 ;ACR先侵犯神经元 ,继之产生远端轴突变性。
Objective To investigate the pathological changes of retrograde necrosis of the axon in C5 7BL / Ola (Ola) mice and normal C5 7BL / 6J (6J) mutants after ACR poisoning and the difference between the two kinds of mice. Relationship between neuronal damage. Methods The changes of neurons in the peroneal nerve, sural nerve and dorsal root ganglion were qualitatively and quantitatively analyzed by light microscopy and electron microscopy. Results The area of total fiber of 6J mice increased obviously under light microscope, the fiber density decreased obviously, the diameter of large diameter fiber decreased; the axons became swollen, the myelin sheath became dark and the shape was irregular. Some dorsal root ganglion cells (A-type cells) nuclear bias to one side, there are some dark particles in the cytoplasm. Electron microscopy showed increased neurofilament within the axon, mitochondria accumulation. Dorsal root ganglion cells mitochondria vacuolar or condensed degeneration. Ola mice showed no significant change. Conclusions Ola rat is delayed in deer-like degeneration induced by ACR. However, axons are swollen and degenerated after 6J poisoning. Neurofilament accumulation and mitochondria accumulation are characterized by electron microscopy. ACR first invades neurons, Followed by the generation of distal axon degeneration.