大鼠健侧颈7神经根移位诱导大脑皮层可塑性变化的分子机制研究

周围神经损伤后相对应的中枢神经也会发生改变。前期研究证实：臂丛神经损伤及修复会导致相应的大脑皮层功能发生可塑性改变；BDNF-TrkB调控下游PLC-γ/CaMKII的信号转导通路在调节突触可塑性和神经再生等过程中发挥重要作用。健侧颈7神经根移位术后出现的患侧与健侧肢体共兴奋的现象通过康复锻炼可逐渐区分，这为研究臂丛神经损伤及修复与中枢神经可塑性变化的相互作用提供了独特的模型。本研究利用健侧颈7神经根移位修复臂丛根性撕脱伤的大鼠模型，通过对比BDNF-TrkB信号通路阻断与否，对于臂丛神经损伤修复后患肢功能恢复的影响，揭示BDNF-TrkB信号通路在健侧颈7神经根移位诱导大脑功能重塑中的作用。如能利用中枢神经可塑性改变的相关机制，则可加快健侧颈7神经根移位后的跨大脑两半球功能重塑，尽早恢复大脑对患肢的自主控制，重建术后瘫痪肢体的功能，进而改善臂丛神经损伤患者的预后，具有重要的临床意义。

After peripheral nerve injury, the corresponding central nervous system will also change. Previous studies have confirmed that brachial plexus injury and repair can lead to plasticity changes in the corresponding cerebral cortex function. BDNF-TrkB regulated PLC-γ/CaMKII signaling pathways plays an important role in regulating synaptic plasticity and nerve regeneration. The co-excitation of affected and healthy limbs can be gradually distinguished by rehabilitation exercise, which provides a unique model for the study of the plasticity changes of central nervous system induced by brachial plexus injury and repair. The purpose of this study is investigating the role of BDNF-TrkB signaling pathway in the functional remodeling of contralateral seventh cervical nerve root transfer in rats with brachial plexus root avulsion by contrasting whether BDNF-TrkB signaling pathway is blocked or not, and the effect of BDNF-TrkB signaling pathway on the functional recovery of affected limbs after brachial plexus nerve injury repair. If the relevant mechanism of central nervous plasticity can be used, the transhemispheric functional remodeling after the transfer of the contralateral seventh cervical nerve root can be accelerated, the autonomic control of the affected limbs can be restored as soon as possible, the function of the paralyzed limbs can be reconstructed, and the prognosis of patients with brachial plexus injury can be improved. It has important clinical significance.