Investigates spontaneous motor recovery in neonatal mice after spinal cord injury, suggesting significant neural adaptations.
Spinal cord injury often causes persistent neurological dysfunction, whereas the developing central nervous system retains greater plasticity. This study investigated whether spontaneous hindlimb motor recovery occurs after complete spinal cord transection in neonatal mice and whether such recovery is accompanied by structural remodeling of the lumbar spinal cord distal to the lesion. C57BL/6J mice underwent complete T9 spinal cord transection at postnatal day 7, and recovery was assessed by Basso Mouse Scale scoring, CatWalk gait analysis, foot-fault testing, immunofluorescence, and electromyography. Compared with adult mice subjected to the same injury, neonatal mice showed progressive partial improvement in hindlimb motor function, including locomotor performance, gait coordination, and foot placement accuracy. Meanwhile, this recovery was accompanied by preservation of lumbar motor neurons and structural changes in the local neural network. Syn+ coverage around lumbar motor neurons was relatively preserved in neonatal injured mice compared with adult injured mice; excitatory synaptic input remained increased, and inhibitory input showed a dynamic pattern of early increase followed by later reduction. In addition, myelin-related alterations were less severe, and motor neuron innervation of peripheral muscles (EMG) were relatively preserved in neonatal mice. The results indicate that the restoration of hindlimb motor function after complete spinal cord transection in neonatal mice is associated with structural and functional remodeling of lumbar spinal motor circuits. This includes enhanced synaptic signals around motor neurons and reorganization of the neuromuscular junction.
No takes yet. Share an insight, caveat, or question.
Peng et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: