The prognosis for substantial and lasting neurological recovery after complete traumatic spinal cord injury (SCI) remains dismal. Disruption of motor and sensory pathways involving not only limb activity, but also respiratory, urinary, and autonomic function, contributes to lifelong morbidity. Obstacles impeding the spinal cord’s ability for self-repair are multifactorial. Principal among these, however, is the limited growth potential of the injured spinal cord, as well as the problematic task of functionally reconnecting supraspinal to spinal neurons, and vice versa. Exciting recent developments in preclinical SCI research, however, are bringing to light novel strategies for circumventing these barriers to spinal recovery with potential for near-future translational therapies. Contrary to traditional thought, axons within the injured adult spinal cord have the capacity to grow, if given optimal circumstances. The propensity for spontaneous axonal growth, however, is limited by the extent of the intrinsic growth potential of adult neurons, and the degree of growth inhibition mediated by the injured cord. A significant component of the inhibitory, internal milieu after injury is due to the presence of chondroitin sulfate proteoglycans (CSPGs) (2, 10). CSPGs are molecules found within the perineuronal net, which have been identified as key factors in preventing axonal growth. Under normal conditions, CSPGs likely function to stabilize mature axons and prevent aberrant growth. After injury, CSPGs are up-regulated at the glial scar that forms at the injury site, and around partially denervated neurons distal to the injury. This increase in CSPGs causes sprouting axons to dieback as they approach the injury epicenter, thereby failing to restore connectivity. Chondroitinase ABC (ChABC) is an enzyme that cleaves the inhibition-mediating sugar chains of CSPGs. In animal models, intraspinal delivery of ChABC has been shown to promote a growth-permissive environment, facilitating spontaneous axonal growth across a spinal cord injury (3, 4). Lasting neurological recovery, however, requires not only axonal growth but also the re-establishment of functional connections between relevant supraspinal and spinal neurons. Precise restoration of point-to-point neural circuitry is a therapeutic challenge that is seemingly unrealistic, particularly of complex long distance neuronal pathways. Increasing recent scientific studies reveal, however, that under ideal conditions, spinal interneurons can sprout new axons after injury. More remarkably, growing