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目的探讨视神经损伤后Bcl2高表达小鼠再生的视神经如何能长入脑内正常的靶组织。方法对生后3d(P3)的C57Bl/6J野生小鼠和Bcl2转基因小鼠进行左眼视神经夹闭损伤,立刻摘除对侧眼球,4d后处死小鼠,做视神经和脑组织切片,评估视神经的再生。视神经损伤后玻璃体内注射一种顺行性标记物———带有荧光的霍乱毒素B(CTBF),来标记视网膜神经节细胞轴突,并在视神经切片上用抗生长相关蛋白43抗体免疫荧光染色显示再生的神经轴突。结果C57Bl/6J小鼠视神经损伤后不能再生,而Bcl2转基因小鼠的视神经活跃地再生了相当长的距离,但再生的视神经轴突不能进入两侧正常的视路,而长入前脑白质。结论生后3d的Bcl2转基因小鼠一侧视神经损伤,同时摘除对侧眼球,去除正常视路的引导后,视神经轴突仍能再生,并可长入脑内,但再生的视神经轴突失去了视路中的引导,不能长入双侧中脑内的靶组织,而是在前脑形成异位神经分布。(中华眼科杂志,2006,42:100103)
Objective To investigate how optic nerve regenerated from Bcl2-overexpressing mice can grow into normal brain tissue after optic nerve injury. Methods C57Bl / 6J wild-type mice and Bcl2 transgenic mice were sacrificed on the third day after implantation (P3), and the contralateral eyeballs were excised immediately. After 4 days, the mice were sacrificed and the optic nerve and brain tissue sections were taken for assessment of optic nerve regeneration. After optic nerve injury, intravitreal injection of a cis-labeled fluorescent cholera toxin B (CTBF) was used to label retinal ganglion cell axons and immunostaining with anti-growth associated protein 43 antibody on optic nerve sections Staining shows regenerated axons. Results C57Bl / 6J mice could not regenerate after optic nerve injury. However, the optic nerve of Bcl2 transgenic mice actively regenerated a considerable distance. However, regenerated axons could not enter the normal visual pathway on both sides and grow into the prefrontal white matter. Conclusion One day after birth, the Bcl2 transgenic mice had optic nerve injury and simultaneous removal of contralateral eyeballs. After removal of normal visual pathway guidance, optic nerve axons could still regenerate and grow into the brain, but regenerated optic nerve axons lost As the guidance in the road, can not grow into the bilateral midbrain target tissue, but in the forebrain to form ectopic nerve distribution. (Chinese Journal of Ophthalmology, 2006,42: 100,103)