Mechanisms that support Raphespinal tract plasticity and regeneration after spinal cord injury

SUMMARY The adult spinal cord is incapable of self-repair after injury or disease, thus leading to lifelong sensory, autonomic, and motor functional deficits. Rehabilitation remains the only effective treatment after CNS trauma, however the anatomical and molecular substrates that support rehab-induced functional re-enforcement and recovery are known. Central to the recovery of voluntary motor function is the capacity for supraspinal circuits to regain access to spinal motor centers. The raphespinal tract (RpST) innervates all spinal lamina and has been shown to be remarkably plastic after spinal cord injury (SCI). Here, we propose to use anatomy, spatial transcriptomics and intersectional in vivo chemogenetics to define the capacity and necessity of intact and lesioned supraspinal RpST terminals to support rehab-induced functional recovery after SCI.