Neurobiology Unit, Department of Experimental Medical Science, Lund University, BMC A11, Solvegatan 17, 22184 Lund, Sweden.
Neuroscience. 2011 Dec 15;198:245-51. doi: 10.1016/j.neuroscience.2011.07.070. Epub 2011 Aug 5.
Positron emission tomography (PET) imaging studies have shown that peak-dose dyskinesia is associated to abnormally high levels of synaptic dopamine (DA) in the caudate-putamen of dyskinetic L-DOPA-treated patients. High striatal extracellular DA levels have also been found in dyskinetic 6-OHDA-lesioned rats as compared to non-dyskinetic ones, suggesting that extracellular DA levels may play a key role in the induction of dyskinesia. In this article we review the evidences pointing to the serotonin system as the primary cause for the abnormally high levels of L-DOPA-derived extracellular DA in Parkinson's disease, and we discuss the feasibility of a therapeutic approach targeting this system.
正电子发射断层扫描（PET）成像研究表明，峰剂量运动障碍与接受高剂量左旋多巴治疗的运动障碍患者尾状核-壳核中突触多巴胺（DA）水平异常升高有关。与非运动障碍大鼠相比，运动障碍的 6-羟基多巴胺（6-OHDA）损伤大鼠纹状体细胞外 DA 水平也升高，这表明细胞外 DA 水平可能在运动障碍的诱导中起关键作用。本文综述了指向 5-羟色胺系统作为帕金森病中异常高的左旋多巴衍生细胞外 DA 水平的主要原因的证据，并讨论了针对该系统的治疗方法的可行性。
