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目的探讨新生小鼠Bcl2高表达是否足以使视神经损伤后再生,并探讨再生的神经轴突能否到达脑内正常的靶组织。方法对出生后3d的C57BL/6J野生小鼠和Bcl2转基因小鼠进行视神经夹闭损伤,1～4d后处死小鼠,做视神经和脑组织切片,利用神经轴突顺行性标记物—带有荧光的霍乱毒素B和GAP43免疫荧光染色检查并评估视神经的再生。结果C57BL/6J野生小鼠视神经损伤后不能再生,损伤的轴突在24h内退缩,而Bcl2转基因小鼠的视神经活跃地再生了相当长的距离,并于4d后到达脑内的靶组织,但大部分再生的神经轴突沿着对侧眼的视路到达损伤同侧的脑内的靶组织,只有很少的神经轴突到达对侧。结论在出生后3d,Bcl2高表达足以使小鼠视网膜神经节细胞损伤后再生,并且再生的神经轴突可以长距离生长至中脑的靶组织,但神经轴突沿着已存在的视路进入同侧的脑内。
Objective To investigate whether high expression of Bcl2 in neonatal mice is sufficient for regeneration after optic nerve injury and to explore whether regenerated axons can reach the normal target tissues in the brain. Methods C57BL / 6J wild-type mice and Bcl2 transgenic mice were sacrificed on the 3rd day after birth and were sacrificed after 1 to 4 days. The optic nerve and brain sections were made. The neuronal axonal markers Fluorescent cholera toxin B and GAP43 immunofluorescence staining and assessment of optic nerve regeneration. Results The C57BL / 6J wild-type mice could not regenerate after optic nerve injury, and the damaged axons shrank within 24 hours. However, the optic nerve of Bcl2 transgenic mice actively regenerated a considerable distance and reached the brain target tissues after 4 days Most of the regenerated axons reach the target tissue in the ipsilateral brain along the visual pathway of the contralateral eye, with very few axons reaching the opposite side. CONCLUSIONS: Bcl-2 overexpression is sufficient to regenerate retinal ganglion cells after 3 days of life, and the regenerated axons can grow to the target tissues of the midbrain over long distances. However, axons protrude along the existing path of vision Ipsilateral brain.