The visual response of retinal ganglion cells is not altered by optic nerve transection in transgenic mice overexpressing Bcl-2
The visual response of retinal ganglion cells is not altered by optic nerve transection in transgenic mice overexpressing Bcl-2
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DOI：
10.1073/pnas.93.25.14955
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发表时间：
1996-12-10
影响因子：
11.1
通讯作者：
Maffei, L
中科院分区：
文献类型：
--
作者：
Porciatti, V;Pizzorusso, T;Maffei, L
将视网膜神经节细胞从逆行性变性中拯救出来的尝试取得了有限的成功，并且存活神经元的残余功能尚不清楚。最近，发现轴突化的视网膜神经节细胞通过凋亡机制死亡。我们使用过度表达 Bcl-2 蛋白（一种强大的细胞凋亡抑制剂）的成年转基因小鼠作为预防体内损伤诱导的细胞死亡的模型。轴切术后几个月，大多数视网膜神经节细胞存活并表现出正常的视觉反应。在对照野生型小鼠中，绝大多数轴突切除的视网膜神经节细胞退化，生理反应消失。这些结果表明，旨在增加 Bcl-2 表达或模拟其功能的策略可能会有效抵消创伤诱导的中枢神经系统细胞死亡。神经元存活是促进再生并最终恢复神经元功能的挑战的必要条件。
Attempts to rescue retinal ganglion cells from retrograde degeneration have had limited success, and the residual function of surviving neurons is not known. Recently, it has been found that axotomized retinal ganglion cells die by apoptotic mechanisms. We have used adult transgenic mice overexpressing the Bcl-2 protein, a powerful inhibitor of apoptosis, as a model for preventing injury-induced cell death in vivo. Several months after axotomy, the majority of retinal ganglion cells survived and exhibited normal visual responses. In control wild-type mice, the vast majority of axotomized retinal ganglion cells degenerated, and the physiological responses were abolished. These results suggest that strategies aimed at increasing Bcl-2 expression, or mimicking its function, might effectively counteract trauma-induced cell death in the central nervous system. Neuronal survival is a necessary condition in the challenge for promoting regeneration and eventually restoring neuronal function.