shRNA干扰PTEN基因对周围神经放大代偿模式下脊髓前、后角突触重塑影响的机制研究

There is axon multiple sprouting grow、mature and reinnervation phenomenon during peripheral nerve axon regeneration process,namely peripheral nerve fibers amplification and compensation effect. The amplification and compensation effect provides new possibilities of applying small nerve to repair big nerve in clinical work. The central system induced by target organ may undergoes bidirectional、mutual、systematic remodeling process and recover the target function when regenerated fibers connected with distal target under peripheral nerve amplification and compensation mode. When PETN gene,(gene of phosphate and tension homology deleted on chromsome ten)was silenced, the synaptic plasticity of spinal cord anterior and dorsal horn may be affected through AKT/mTOR signal pathway, and the axons regeneration velocity、the axons regeneration amplification and compensation limit、the target organ functional recovery were all improved significantly. The research of structural and functional remodeling under peripheral nerve amplification and compensation mode, may help to understand the peripheral nerve regeneration process from the pathological and physiological view;and accomplish the possibilities of applying small nerve to repair big nerve to the greatest extent in specific injury classification.

周围神经轴突的再生过程中存在轴突多芽生长、成熟、再支配现象，即神经纤维的放大代偿效应。周围神经的放大代偿效应提示了临床上以细小神经修复粗大神经的可行性。周围神经放大代偿模式下的再生纤维与远端效应器连接后，中枢神经系统将在末梢效应器的诱导下进行双向、交互、系统重塑并恢复相应末梢效应器的功能。.第10号染色体缺失的磷酸酶及张力蛋白同源基因（gene of phosphate and tension homology deleted on chromsome ten, PTEN）沉默后，可能通过AKT/mTOR等信号通路影响到脊髓前、后角突触重塑的过程，并加快周围神经轴突的再生速度，提高轴突再生的放大代偿极限，促进神经再支配靶器官的功能恢复。放大代偿修复模式下结构和功能重塑的研究，有助于从病理生理角度重新认识神经损伤修复后的再生过程；最大程度的实现特定的损伤类型中以细小神经修复粗大神经的可能性。

周围神经轴突的再生过程中存在轴突多芽生长、成熟、再支配现象，即神经纤维的放大代偿效应。周围神经的放大代偿效应提示了临床上以细小神经修复粗大神经的可行性。周围神经放大代偿模式下的再生纤维与远端效应器连接后，中枢神经系统将在末梢效应器的诱导下进行双向、交互、系统重塑并恢复相应末梢效应器的功能。.第10号染色体缺失的磷酸酶及张力蛋白同源基因（gene of phosphate and tension homology deleted on chromsome ten, PTEN）沉默后，可能通过AKT/mTOR等信号通路影响到脊髓前、后角突触重塑的过程，并加快周围神经轴突的再生速度，提高轴突再生的放大代偿极限，促进神经再支配靶器官的功能恢复。放大代偿修复模式下结构和功能重塑的研究，有助于从病理生理角度重新认识神经损伤修复后的再生过程；最大程度的实现特定的损伤类型中以细小神经修复粗大神经的可能性。