痉挛是脊髓损伤后常见的症状，运动神经元对单胺的敏感性增强被认为是痉挛发生的主要机制。芳香族氨基酸脱酸酶（AADC）是催化5 - 羟色氨酸转化为5-羟色胺（5 – HT）、左旋多巴转化成多巴胺（DA）的一种必需酶。传统观念认为脊髓组织中的AADC没有活性，我们近期研究取得突破性进展，首次发现脊髓损伤能诱导AADC细胞发生表型转变合成5-HT/DA，并发现脊髓损伤诱导AADC细胞产生5-HT的机制与5-HT自身受体5-HT1B相关。那么为什么脊髓损伤后AADC细胞能够发生表型改变合成DA？在痉挛的发生发展中AADC 细胞又发挥怎样的作用？不同节段脊髓损伤后AADC细胞是否发生相同的表型改变？本项目重点研究以上问题，旨在进一步揭示痉挛发生机制，为临床脊髓损伤后的康复治疗提供新思路。

Spasticity is a common symptom following spinal cord injury (SCI), the underlying mechanism is unclear but supersensitivity of motor neurons to monoamines is believed to be a major cause. AADC is the enzyme that catalyzes the decarboxylation of 5-hydroxytryptophan (5-HTP) to 5-HT and L-dopa to dopamine(DA). AADC positive cells in the spinal cord are usually inactive, but are activated post-SCI and undergo a phenotypic change to produce 5-HT/DA, we have previously found that 5-HT1B receptors play an important role in the enhanced ability of AADC cells to produce 5-HT.Thus in this project, we try to answer the following questions: What is the possible mechanism for the phenotypic change of AADC cells to produce DA after spinal cord injury? What is the action of AADC cells in the pathogenesis of spasticity after spinal cord injury? We ask whether AADC cells have the same phenotypic change in different level of spinal cord injury. The aim of our study is to investigate the mechanism of spasticity and to provide new clue for clinical treatment.