We previously showed that Nuclear Factor κB (NF‐κB) inactivation in astrocytes leads to improved functional recovery following spinal cord injury (SCI). This correlated with reduced expression of pro‐inflammatory mediators and chondroitin sulfate proteoglycans, and increased white matter preservation. Hence we hypothesized that inactivation of astrocytic NF‐κB would create a more permissive environment for axonal sprouting and regeneration. We induced both contusive and complete transection SCI in GFAP‐Inhibitor of κB‐dominant negative (GFAP‐IκBα‐dn) and wild‐type (WT) mice and performed retrograde [fluorogold (FG)] and anterograde [biotinylated dextran amine (BDA)] tracing 8 weeks after injury. Following contusive SCI, more FG‐labeled cells were found in motor cortex, reticular formation, and raphe nuclei of transgenic mice. Spared and sprouting BDA‐positive corticospinal axons were found caudal to the lesion in GFAP‐IκBα‐dn mice. Higher numbers of FG‐labeled neurons were detected immediately rostral to the lesion in GFAP‐IκBα‐dn mice, accompanied by increased expression of synaptic and axonal growth‐associated molecules. After transection, however, no FG‐labeled neurons or BDA‐filled axons were found rostral and caudal to the lesion, respectively, in either genotype. These data demonstrated that inhibiting astroglial NF‐κB resulted in a growth‐supporting terrain promoting sparing and sprouting, rather than regeneration, of supraspinal and propriospinal circuitries essential for locomotion, hence contributing to the improved functional recovery observed after SCI in GFAP‐IκBα‐dn mice.