Salzman S K, Knight P B, Hirofuji E, Llados-Eckman C, Beckman A L, Winokur A
Peptides. 1987 Mar-Apr;8(2):247-50. doi: 10.1016/0196-9781(87)90098-2.
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.
研究了撞击诱导的脊髓损伤对脊髓中免疫反应性促甲状腺激素释放激素（TRH-ir）浓度的影响。在撞击后30分钟、1小时、4小时和6周，从损伤部位近端、远端及损伤部位取材。在损伤后30分钟时，损伤部位的TRH-ir最初减少了38%，之后所有部位的浓度均随时间逐渐升高。创伤后4小时，近端和远端节段的这些升高达到统计学显著水平。到6周时，观察到TRH-ir浓度呈头-尾梯度变化，表明轴浆运输受到限制。该梯度的特征是损伤近端TRH-ir显著升高，损伤远端减少60%。所测得的短期TRH-ir升高表明，外源性给予TRH降低创伤后功能缺陷发生率的能力源于内源性TRH作用的恢复。同时也考虑了中缝脊髓束在创伤性麻痹发生中的作用。
