期刊
EMBO REPORTS
卷 14, 期 10, 页码 931-937出版社
WILEY
DOI: 10.1038/embor.2013.117
关键词
axonal remodelling; corticospinal tract; neuronal plasticity; spinal cord injury; STAT3
资金
- Deutsche Forschungsgemeinschaft [SFB 870]
- Federal Ministry of Education and Research (BMBF, Independent Groups in the Neurosciences)
- DFG [SFB 870, SFB-Tr 128]
- BMBF (Competence Network Multiple Sclerosis)
- European Research Council under the European Union's Seventh Framework Program (ERC) [310932]
- Hertie Foundation
- Verein 'Therapieforschung fur MS-Kranke e.V.'
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.
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