肢体痉挛是脊髓损伤后最严重的并发症之一，然其发生神经机制仍不清楚。基于前期研究中意外发现在运动下行传导束如皮质脊髓束（CST）损伤后出现自发性再生同时，脊髓中间神经元（PST）也显示出“出芽”较强的再生能力, 并与CST环路重建发挥重要的可塑性代偿作用。因此本研究拟将通过Celsr3|Emx1条件基因敲除构建皮质脊髓束（CST）遗传缺失小鼠模型，在中间神经（PST）传导通路仍保持正常下研究其可塑性变化，并用顺行和逆行性示踪剂标志PST,分析PST神经轴突、树突形态、轴突分布及PST与上下神经元的环路重建情况，提出并验证假说：脊髓损伤后肢体痉挛是由于PST兴奋性发生改变;神经出芽形成的新突触、错配建立新的错配神经通路，是导致支配区域肌肉痉挛的重要神经新机制具有重要意义。

Spasticity is one of the most serious complication after spinal cord injury,but the incidence of neural mechanism is not clear.In our previous study,we accidentally found that after injury of moving downward conduction bundle such as CST,spinal interneurons (PST) showed a strong ability of regeneration called bud and reconstrcted CST loop to play an important role in the plasticity of compensation as well as CST regenerated spontaneously.So the study intends to construct the CST genetic deletion mouse model under conditional knockouting of Celsr3|Emx1,then study its plasticity when the middle of the nerve (PST) pathway remained normal and mark PST with the anterograde and retrograde tracer to analysis the form of axons or dendrites,axons distribution and the loop reconstruction of PST and the upper and lower neuron.What's more,propose and validate hypothesis:Limb spasticity after spinal cord injury is due to excitability change of PST;New synapses come by nerve sprouting and mismatch formation of new neural pathways lead to a new important neural mechanism of the muscle spasm in regional dominance,which has important significance.