Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells
Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells
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DOI：
10.1126/science.1068428
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发表时间：
2002-06-07
期刊：
影响因子：
56.9
通讯作者：
Barres, BA
中科院分区：
文献类型：
--
作者：
Goldberg, JL;Klassen, MP;Barres, BA
中枢神经系统（CNS）在发育早期失去再生能力，但原因尚不清楚。长期以来，视网膜一直是研究CNS再生的简单模型系统。在这里，我们表明，无长突细胞信号新生大鼠视网膜[神经节细胞（RGCs）进行深刻的和显然不可逆的损失内在轴突生长能力。同时，视网膜。成熟触发RGC大大增加其树突生长能力。这些结果表明，成年中枢神经系统神经元不能再生不仅是因为中枢神经系统胶质细胞的抑制，但也因为内在轴突生长能力的损失。
The central nervous system (CNS) loses the ability to regenerate early during development, but it is not known why. The retina has long served as a simple model system for study of CNS regeneration. Here we show that amacrine cells signal neonatal rat retina[ ganglion cells (RGCs) to undergo a profound and apparently irreversible loss of intrinsic axon growth ability. Concurrently, retinal. maturation triggers RGCs to greatly increase their dendritic growth ability. These results suggest that adult CNS neurons fail to regenerate not only because of CNS glial inhibition but also because of a loss of intrinsic axon growth ability.