L1 overexpression in rats with complete spinal cord transection downregulates phosphacan and upregulates synaptophysin, GAP43 and Adcy1 expression

Recovery after spinal cord injury requires neuronal remodeling which is regulated by cell adhesion molecules (CAMs) and chondroitin sulfate proteoglycans (CSPGs). CSPG may be potentially both inhibitory and supportive of regenerative plasticity. To verify whether chronic (5 weeks) L1 CAM overexpression in transected spinal cord of the rat, proven to promote recovery in mice, affects CSPG phosphacan and markers of synaptic plasticity, adeno-associated viral vector encoding L1 protein (AAV5-L1) was injected into L1 lumbar segment, immediately after transection at Th10/11. Control group received AAV5-EGFP. AAV5-L1 transduced neurons and astrocytes below the lesion, resulting in 170-fold increase in L1 mRNA level at low thoracic segments (Th