脊柱胸腰段骨折在临床上最为常见，损伤后可导致排尿、排便功能障碍。其肠道症状主要表现为严重大便失禁，慢性顽固性便秘等。本课题组前期在国家自然基金青年项目（30901507）的资助下，首先定位大鼠排便的初级运动、感觉中枢；应用神经移位同时修复直肠与肛管的运动、感觉神经，从而建立了生理排便反射通路。但是新的反射通路能否与大脑中枢建立联系尚不明确。因此，本研究拟以大鼠为研究对象，通过跨突触逆行示踪、微电极刺激、功能磁共振成像、PET显像等方法，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，并通过测定脑源性神经生长因子（BDNF）、生长相关蛋白43（GAP43）、非受体酪氨酸激酶(Fyn)和Trk酪氨酸激酶B(TrkB) mRNA 及其蛋白在相关脑功能区的表达，从而探讨人工反射通路修复术后大脑重塑的分子机制，可望为临床上脊髓损伤患者实现自主排便奠定实验基础。

Thoracolumbar fracture was common in clinic, which might induce to the disorders of urination and defecation. The disorder of defecation might mainly manifest severe fecal incontinence and chronic intractable constipation. Funded by the National Natural Science Foundation of China (Grant No.30901507), the primary motor and sensory centers were located in rats firstly. Then the repairments of motor and sensory pathways in the rectum and anal canal were performed simultaneously with nerves tranferring. Thus the defecation reflex was established. However, the functional reorganization in rat brain after reconstructed with the new physiological reflex pathway is not yet clear. Therefore, the outcome of functional reorganization will be testified with inter-synaptic retrograde nerve tracing, micro-electrode stimulation and functional magnetic resonance imaging (f MRI), 18F-FDG PET imaging. Thus the functional reorganization changes in the defecation senior center (which included paracentral lobule, hypothalamus and brain- stem) were detected. mRNA and protein expression of brain-derived neurotrophic factor (BDNF), growth associated protein 43 (of GAP43) , non-receptor tyrosine kinase (Fyn) and Trk tyrosine kinase B (TrkB) in the functional areas were measured, which might explore the molecular mechanisms of brain functional reorganization. And this study might offer an experimental foundation to achieve autonomic defecation for the patients after spinal cord injury.