脊髓损伤可导致损伤平面以下运动、感觉障碍以及排尿排便功能障碍。随着对泌尿系统处理方法的进步，使肠道功能障碍的影响日益突出。本课题组在前期研究中，应用神经移位建立了生理排便反射通路。但是新的生理反射通路建立后大脑重塑的机制尚不明确。本研究拟以大鼠为研究对象，通过跨突触逆行示踪、经颅磁刺激、7.0T功能磁共振成像等方法，来观测排便高级中枢——旁中央小叶，丘脑下部及脑干在人工反射通路修复前后的迁移变化规律；并通过脑双位点微透析结合高效液相色谱分析，动态监测神经核团内胆碱类神经递质的含量变化；并测定I型主要组织相容性复合体（MHCI），NF-κB p65及其上游抑制因子IκB，以及蛋白激酶PKMζ、PKCλ在相关脑功能区的表达，进而从神经递质、免疫网络及信号通路等角度来探讨人工排便反射通路修复术后大脑重塑的可能机制，从而可望为临床上脊髓损伤患者实现自主排便奠定实验基础。

Spinal cord injury (SCI) could result in dysfunction of motor, sensation, urination and defecation below the level of the injury. Bowel dysfunction becomes increasingly prominent following the advancement of treatment to urinary dysfunction. In the previous research by our group, a reflex pathway for defecation was reconstructed by nerve transfer. However, the mechanisms of brain plasticity after reconstruction of the new reflex pathway remain unclear. Rats are chosen as the research animal in this study. By using trans-synaptic retrograde neural tracing, transcranial magnetic stimulation (TMS) and 7.0T fMRI , the changes of the central nervous system controlling defecation (paracentral lobule, hypothalamus and brainstem) will be detected. Cholinergic neurotransmitter in the nucleus will be detected dynamically by brain double-site microdialysis combined with high performance liquid chromatography. Meanwhile, expression of class I major histocompatibility complex (MHCI), NF-κB p65, inhibitory factor IκB, protein kinase M ζ (PKMζ) and protein kinase C λ (PKCλ) in corresponding brain functional area will also be tested. In this way, the molecular mechanism and signal pathway underlying artificial reflex pathway reconstruction will be explored with the aspects of neurotransmitter, immunological network and signal pathway, which may provide experimental basis for patients with SCI to achieve autonomic defecation.