Institute of Clinical Neuroimmunology, Ludwig-Maximilians Universität, Marchioninistrasse 17, Munich 81377, Germany.
EMBO Rep. 2013 Oct;14(10):931-7. doi: 10.1038/embor.2013.117. Epub 2013 Aug 9.
If and how neurons remodel their connections after CNS injury critically influences recovery of function. Here, we investigate the role of the growth-initiating transcription factor STAT3 during remodelling of the injured corticospinal tract (CST). Endogenous STAT3 expression in lesioned cortical projection neurons is transient but can be sustained by viral gene transfer. Sustained activation of STAT3 enhances remodelling of lesioned CST fibres and induces de novo formation of collaterals from unlesioned CST fibres. In a unilateral pyramidotomy paradigm, this recruitment of unlesioned fibres leads to the formation of midline crossing circuits that establish ipsilateral forelimb activation and functional recovery.
如果和中枢神经系统损伤后神经元如何重塑它们的连接,严重影响功能的恢复。在这里,我们研究了增长启动转录因子 STAT3 在损伤皮质脊髓束 (CST) 重塑过程中的作用。内源性 STAT3 表达在损伤的皮质投射神经元是短暂的,但可以通过病毒基因转移来维持。STAT3 的持续激活增强了损伤 CST 纤维的重塑,并诱导来自未损伤 CST 纤维的侧支的新生形成。在单侧锥体切开术模型中,这种未损伤纤维的募集导致中线交叉回路的形成,从而建立同侧前肢激活和功能恢复。