成年肌萎缩脊髓侧索硬化症转基因鼠脊髓增殖细胞的分化

目的 探讨成年肌萎缩脊髓侧索硬化症(ALS)转基因模型鼠脊髓内增殖细胞的类型及分化情况. 方法 对ALS转基因鼠发病期进行BrdU标记,分别于不同时间点取材,冷冻切片,应用免疫荧光双标及三标染色技术检测ALS转基因鼠病变进展过程中脊髓内增殖细胞的分化情况. 结果 成年ALS转基因鼠发病期脊髓的中央管、灰质、白质均未检测到BrdU/DCX双标记阳性细胞和BrdU/NeuN双标记阳性细胞.灰质、白质和中央管周围检测到大量NG2阳性细胞,阳性细胞数量随病变进展逐渐减少,NG2阳性细胞多呈BrdU阳性表达;可检测到少量BrdU/A2B5双标记阳性细胞;ALS转基因鼠发病期脊髓BrdU/GFAP双标记阳性细胞较多,部分双阳性细胞呈Nestin阳性,而野生型鼠脊髓内未检测到BrdU/GFAP双标记阳性细胞.结论 神经退行性病变激活ALS转基因鼠脊髓内源性增殖细胞向神经胶质细胞方向分化,未检测到向神经元方向分化,内源性增殖细胞尚不能有效地促进退行性病变的修复.

Study on the cellular differentiation of the proliferating cells in the spinal cord of adult amyotrophic lateral sclerosis transgenic mice

Objective To explore the characteristic and differentiation of the proliferating cell in the spinal cord of adult amyotrophic lateral sclerosis(ALS) transgenic mice. Methods BrdU was injected at different time points during the symptomatic stage of the disease, and frozen sections were made. The cell characteristic and differentiation of the proliferating cell in the spinal cords of adult ALS transgenic mice were detected using double and triple immunofluorescence labeling technology. Results None BrdU/NeuN or BrdU/DCX double labeling cells were found in the central canal, gray matter and white matter of adult ALS transgenic mice spinal cord during the symptomatic stage of the disease. There were significantly NG2 labeling cells in the central canal, gray matter and white matter, expressing cells were detected a reduction in number during the symptomatic stage of the disease, and NG2 was expressed by most BrdU-labeled cells; Colocalization of A2B5 and BrdU was also detected in ALS mice. There were many BrdU/ GFAP double positive cells in the spinal cord of adult ALS transgenic mice, some were nestin positive, No BrdU/GFAP double labeling cells were found in wild type mice. Conclusion The neurodegenerative process stimulates a regenerative response, and there is significantly increased gliogenesis but absence of convincing neurogenesis. These data suggest that endogenous neural regeneration is insufficient for compensating the neurodegeneration.