Abstract: Traumatic injuries to the central nervous system (CNS) result in disruptton of the intricate network of axons which connect functionally related neurons that are widely distributed throughout the brain and spinal cord. Under normal conditions, maintenance of this complex system is structurally and functionally supported by astrocytes (ACs) and other glial cells, the processes of which form a framework surrounding neuronal cell bodies, dendrites, axons, and synapses. Following injury, however, ACs adopt a reactive, scar-forming phenotype to establish a barrier that limits the spread of inffammatory cells and molecules from the primary lesion site to adjacent nervous ttssue, effecttvely limittng secondary ttssue degeneratton. Unfortunately, due to the persistent nature of the resulttng glial scar, this inittally protecttve functton acts as a double-edged sword as it also suppresses CNS axon sprouting and regeneration across the lesion site, resulting in permanent disability for those affected.