| Functional recovery after spinal cord injury requires axons to overcome inhibitory factors, grow beyond the lesion site, and synapse on the appropriate target. We investigated whether developmental pathways necessary for axon differentiation and growth persist in the mature nervous system. We tested the hypothesis that manipulations of developmentally important neuronal TGF-beta signaling would affect adult axonal regeneration following injury. We found that, in contrast to development, TGF-beta inhibits growth of adult neurons and over-expression of SnoN, a developmentally regulated transcription factor that inhibits TGF-beta signaling, rescues adult neurons from TGF-beta induced inhibition. More importantly, SnoN over-expression in sensory neurons was sufficient to enhance axon regeneration into a cell graft placed in the lesion cavity in an in vivo model of spinal cord injury. |
