Carta Manolo, Carlsson Thomas, Muñoz Ana, Kirik Deniz, Björklund Anders
Neurobiology Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Prog Brain Res. 2008;172:465-78. doi: 10.1016/S0079-6123(08)00922-9.
Appearance of dyskinesia is a common problem of long-term Levodopa (L-DOPA) treatment in Parkinson's disease (PD) patients and represents a major limitation for the pharmacological management of the motor symptoms in the advanced stages of disease. An increasing body of evidence points to dopamine released as a false neurotransmitter from the striatal serotonin terminals as the main pre-synaptic determinant of L-DOPA-induced dyskinesia. Here we review the animal experimental and human clinical data in support of this view, which point to the serotonin system as a promising target for anti-dyskinetic therapy in PD patients under L-DOPA medication.
运动障碍的出现是帕金森病(PD)患者长期左旋多巴(L-DOPA)治疗中常见的问题,也是疾病晚期运动症状药物治疗的主要限制因素。越来越多的证据表明,从纹状体5-羟色胺末端释放的作为假神经递质的多巴胺是L-DOPA诱导的运动障碍的主要突触前决定因素。在此,我们综述了支持这一观点的动物实验和人类临床数据,这些数据表明5-羟色胺系统是接受L-DOPA药物治疗的PD患者抗运动障碍治疗的一个有前景的靶点。