视网膜神经节细胞通过无长突细胞信号传导导致内在轴突生长能力丧失。

Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells.

作者信息

Goldberg Jeffrey L, Klassen Matthew P, Hua Ying, Barres Ben A

机构信息

Stanford University School of Medicine, Department of Neurobiology, Sherman Fairchild Science Building D231, 299 Campus Drive, Stanford, CA 94305-5125, USA.

出版信息

Science. 2002 Jun 7;296(5574):1860-4. doi: 10.1126/science.1068428.

DOI:10.1126/science.1068428

PMID:12052959

Abstract

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 retinal 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.

摘要

中枢神经系统（CNS）在发育早期就失去了再生能力，但原因尚不清楚。长期以来，视网膜一直是研究中枢神经系统再生的一个简单模型系统。在这里，我们表明无长突细胞向新生大鼠视网膜神经节细胞（RGCs）发出信号，使其内在轴突生长能力发生深刻且明显不可逆的丧失。同时，视网膜成熟促使RGCs极大地提高其树突生长能力。这些结果表明，成年中枢神经系统神经元无法再生不仅是因为中枢神经系统胶质细胞的抑制，还因为内在轴突生长能力的丧失。