Cortex-dependent recovery of unassisted hindlimb locomotion after complete spinal cord injury in adult rats.
After paralyzing spinal cord injury the adult nervous system has little ability to 'heal' spinal connections, and it is assumed to be unable to develop extra-spinal recovery strategies to bypass the lesion. We challenge this assumption, showing that completely spinalized adult rats can recover unassisted hindlimb weight support and locomotion without explicit spinal transmission of motor commands through the lesion. This is achieved with combinations of pharmacological and physical therapies that maximize cortical reorganization, inducing an expansion of trunk motor cortex and forepaw sensory cortex into the deafferented hindlimb cortex, associated with sprouting of corticospinal axons. Lesioning the reorganized cortex reverses the recovery. Adult rats can thus develop a novel cortical sensorimotor circuit that bypasses the lesion, probably through biomechanical coupling, to partly recover unassisted hindlimb locomotion after complete spinal cord injury.
['Manohar|Anitha|A|0000-0002-3011-2623', 'Foffani|Guglielmo|G|', 'Ganzer|Patrick D|PD|', 'Bethea|John R|JR|', 'Moxon|Karen A|KA|0000-0002-5790-097X']
D000818:Animals D001369:Axons D006614:Hindlimb D008124:Locomotion D009044:Motor Cortex D051381:Rats D020127:Recovery of Function D013119:Spinal Cord Injuries
rat cortex SpinalCord neuroscience plasticity