Spinal cord immunoreactive TRH is altered after local traumatic injury.
The effect of impaction-induced spinal trauma on the concentration of immunoreactive TRH (TRH-ir) in the spinal cord was studied. Samples were obtained from tissues proximal to, distal to, and at the site of injury at 30 min, 1 hr, 4 hr, and 6 weeks after impaction. After an initial 38% depletion of TRH-ir at the injury site at 30 min, concentrations were progressively elevated over time at all sites. These elevations reached statistical significance in the proximal and distal segments by 4 hr posttrauma. By 6 weeks, a rostral-caudal gradient of TRH-ir concentration was observed, indicating that axoplasmic transport was restricted. The gradient was characterized by a significant TRH-ir elevation proximal to, and a 60% depletion distal to, the injury. The short-term TRH-ir elevation measured indicates that the ability of exogenously administered TRH to reduce the incidence of posttraumatic functional deficit stems from a restoration of endogenous TRH action. The role of the raphe-spinal tract in the development of traumatic paralysis is considered.
D000818:Animals; D009928:Organ Specificity; D010264:Paraplegia / Q000378:metabolism; D011817:Rabbits; D013116:Spinal Cord / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*
D013973:Thyrotropin-Releasing Hormone