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目的 研究大鼠脊髓全横断后脑源性神经营养因子 (BDNF)及其高亲和力受体 (TrkB)在运动皮质表达的变化 ,为进一步探索脊髓损伤后再生修复机制和神经营养因子治疗脊髓损伤提供实验依据。 方法 雄性SD大鼠 4 2只随机分为 3组 :1 脊髓横断组 :动物脊髓在胸 9节段完全横断 ,按存活时间不同分为术后 3、7、14、2 1及 2 8d组 ;2 假手术组 (只行椎板切除术 ) ;3 正常对照组。动物到达存活时间点后 ,应用免疫组织化学ABC方法和图像分析技术检测TrkB及BDNF在运动皮质的表达和分布。 结果 对照组和实验组运动皮质TrkB和BDNF阳性细胞主要分布在第 5层 ,第 3、4、6层也有少量阳性细胞。脊髓全横断后TrkB和BDNF的表达逐渐增高 ,于术后 2 1d达高峰 ,2 8d回到正常水平 ,且TrkB表达上调早于BDNF。 结论 脊髓全横断后运动皮质对BDNF的需求增加 ,内源性BDNF的增加可能有利于受损的皮质脊髓束神经元的存活与再生 ;在损伤早期给予外源性BDNF可能更有利于受损的皮质脊髓束神经元。
Objective To investigate the changes of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor (TrkB) in the motor cortex after spinal cord transection, and to provide experimental evidence for further exploring the mechanism of regenerative repair and neurotrophic factor in spinal cord injury after spinal cord injury in accordance with. Methods Male Sprague-Dawley rats were randomly divided into 3 groups: (1) spinal cord transection group: The animal spinal cord was transected completely in the thoracic segment 9 and divided into 3, 7, 14, 21, and 28 d groups according to the survival time; 2 sham operation group (only laminectomy); 3 normal control group. After reaching the point of survival, the expression and distribution of TrkB and BDNF in motor cortex were detected by immunohistochemical ABC method and image analysis technique. Results The TrkB and BDNF positive cells in the motor cortex of the control group and the experimental group were mainly distributed in the fifth layer and a small amount of positive cells in the third, fourth and sixth layers. The expression of TrkB and BDNF increased gradually after spinal cord transection, reaching the peak on the 21st day after operation and returned to the normal level on 28th day. The up-regulation of TrkB was earlier than that of BDNF. Conclusions The demand of BDNF is increased in motor cortex after fully transected spinal cord. Increased endogenous BDNF may be beneficial to the survival and regeneration of injured corticospinal tract neurons. Exogenous BDNF may be more beneficial to impaired Corticospinal tract neurons.