Elucidation of neuronal regenerative mechanism after ischemia and its modulation therapy

本研究采用大鼠全脑缺血模型，探讨外源性生长因子是否能促进纹状体神经元选择性死亡。结果，纹状体神经元密度在缺血后2天下降至1%，经生长因子处理后，纹状体神经元密度最终上升至12-15%。用BrdU标记分化神经祖细胞，这些细胞的后代分布在纹状体中，分化为特定区域的突起和神经元间。此外，这些细胞在缺血20周后电生理成熟。运动性能也显著提高。综上所述，这些结果表明，内源性神经元再生的调节可以通过治疗增强，并最终导致功能恢复。

Here we explored whether neuronal regeneration can be augmented by administration of exogenous growth factors by using rat global ischemia model, which induced selective neuronal death in the striatum. As a result, neuronal density in the striatum decreased to 1% by 2 days after ischemia, that was finally increased to 12-15% by the growth factor treatment. When dividing neural progenitors were labeled by BrdU, the progeny of these cells were distributed in the striatum, differentiated into region specific projection and inter-neurons. In addition, these cells maturated electrophysiologically after 20 weeks of ischemia. Motor performance also improved significantly. Collective, these results suggested that the modulation of endogenous neuronal regeneration can be potentiated by the treatment, and finally leads to functional recovery.