Research ArticleSpinal Cord Injury

Cbp-dependent histone acetylation mediates axon regeneration induced by environmental enrichment in rodent spinal cord injury models

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Science Translational Medicine  10 Apr 2019:
Vol. 11, Issue 487, eaaw2064
DOI: 10.1126/scitranslmed.aaw2064

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An epigenetic mechanism for regenerating axons

Functional recovery after spinal cord injury (SCI) is limited by lack of axon regeneration in the mature nervous system. However, recent data showed that increasing neuronal activity promoted axonal regeneration after SCI in rodents. In a new study, Hutson et al. investigated the mechanisms mediating activity-dependent neuronal response in rodent models of spinal cord injury. Increasing neuronal activity using chemical or behavioral approaches promoted recovery through Creb-binding protein (Cbp)–mediated histone acetylation, and using a small-molecule Cbp activator mimicked the effects of increasing neuronal activity. This epigenetic mechanism might be exploited for enhancing repair and functional recovery after SCI.

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