Introduction

This chapter is devoted to mechanisms of spinal cord plasticity in animal models as revealed by the recovery of motor functions after a spinal lesion. It will be shown that in cats, rats and mice, motor programs such as locomotion are re-expressed after a complete spinal transection at the low-thoracic level. This suggests that the main neural networks at the basis of these motor programs reside in the spinal cord. Direct evidence for the operation of these circuits as well as cellular properties implicated will be surveyed. On the other hand, modifications of these motor programs by sensory inputs, training and pharmacological stimulation suggest that some of the control mechanisms have some degree of plasticity. Obviously, supraspinal structures normally play a crucial role in the purposeful goal-orienting control of these spinal pattern generators. The deficits observed after complete or partial spinal lesions of ventral/ventrolateral or dorsolateral tracts reveal indeed these important roles. Altogether, these observations lead to the important concept that complex motor functions such as locomotion are largely subserved by intrinsic spinal mechanisms under segmental and suprasegmental controls that are plastic enough to justify the use of rehabilitation approaches to optimize functional locomotor recovery after spinal lesions. Figure 13.1 schematizes the principal structures and mechanisms that will be discussed in this chapter. For related discussions, see Volume I, Chapters 7 and 30, and Volume II, Chapters 3 and 19.