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.

Grant Number: 1R21NS139481-01A1
NIH Institute/Center: NIH
Principal Investigator: William Cafferty