One cause of regenerative failure observed after spinal cord injury is the expression of repulsive factors at the injury site. Eph receptors and their ligands, the ephrins, are candidates that could mediate inhibitory effects on axonal regeneration, since these molecules mediate contact-dependent inhibitory signals that regulate axonal pathfinding and tissue patterning during development. However, little is known about the function of the ephrin/Eph system after CNS injury in the adult. Previously, we reported that after thoracic spinal cord transection in adult rats, EphB2 protein levels increased at the lesion 1-2 weeks after injury (Bundesen et al., SFN Abstr. 2000). Immunohistochemistry revealed that EphB2 was expressed by fibroblasts infiltrating the lesion site. In the present study, we observed that ephrinB2, a ligand for EphB2, was strongly expressed by astrocytes at the glial scar. No intermingling of EphB2-positive fibroblasts and ephrinB2-positive astrocytes was observed. Thus, we propose that r...