Animal models of damage, repair, and plasticity in the spinal cord

Sensorimotor function can improve for years, even after a spinal cord injury (SCI). We also know that an effective intervention that can improve motor function is re-engagement of the spinal neural networks through supraspinal control and that this regularity in re-engagement is fundamental to learning within the activated sensorimotor circuits. Several interventions, ranging from monoclonal antibodies against neurit outgrowth inhibitors to epidural electrical stimulation, have been developed allowing individuals with a SCI to re-engage sensorimotor circuits. These interventions enable spinal neural circuits to neuromodulate the level of excitability closer to a near motor threshold state. This is because of the built-in level of automaticity within the spinal circuits that then is translated into motor commands specified by the sensory input. Another increasingly apparent feature of the spinal circuitry is the highly integrated nature of multiple physiological systems linked to load bearing sensory input. Thus, it is clear that multiple physiological systems are highly responsive to activity-dependent interventions after a severe SCI and that this responsiveness can persist for years post-injury and be therapeutically modulated.