This chapter discusses the mechanisms of spinal cord plasticity in animal models as revealed by the recovery of motor functions after a spinal lesion. It shows that in cats, rats and mice, motor programs such as locomotion are re-expressed after a complete spinal transection at the low-thoracic level. The pharmacological work with intrathecal cannula suggested that important effects on locomotion could be observed when the intrathecal injections were localized to the rostral spinal segments. Clinically, the notion that certain spinal segments may play a critical role in the control of spinal locomotion may help to somewhat simplify where to target pharmacological stimulation, cell grafts or electrical stimulation. With the advent of genetic characterization and the potential for genetic manipulations, the mouse is becoming an increasingly important model for spinal cord injury research. The characteristics of motor patterns result from an intricate dynamic sensori-motor interaction between the spinal and supraspinal levels.

Interest in activity-dependent spinal cord plasticity is increasing with the growing recognition that the acquisition and maintenance of normal motor performances reflect activity-dependent plasticity at multiple sites throughout the central nervous system (CNS), including the spinal cord. This chapter addresses the range of activity-dependent plasticity during normal life. The behavioral effects associated with spinal cord plasticity appear to reflect the interaction of plasticity at both spinal and supraspinal sites. The substantial capacity for activity-dependent plasticity in the spinal cord has important theoretical and practical implications. The substantial capacity suggests that most motor skills that are acquired gradually through prolonged practice involve spinal cord plasticity. The ubiquity of activity-dependent plasticity and the inevitable interaction between primary, compensatory, and reactive types, implies that functional effects may change over time. Early gains will not always evolve into long-term improvements, while deleterious early effects may give way to long-term benefits.