持续的研究已经证实高频电针能有效改善帕金森病（PD）的运动症状，但其中枢作用机制尚不清楚。最新研究揭示，针对运动皮层的治疗能改善PD运动症状，与其干扰了皮层-基底节通路中异常同步化震荡活动直接相关。预实验表明电针能调节皮层神经元放电及谷氨酸的释放，因而提出"电针是以运动皮层为调控靶点，通过对谷氨酸介导的皮层神经元兴奋/抑制的平衡调节，以及对皮层-基底节通路中同步化震荡活动的调控而改善PD运动症状"。以深部脑刺激和去皮层处理为对照，检测电针对大鼠行为学、皮层神经元放电的影响来证实电针的作用靶点；采用清醒动物在体多通道技术，同步记录皮层与基底节各核团的局部场电位和峰电位，分析电针对核团间同步化震荡活动的影响来明确电针的调控途径；检测皮层及核团的谷氨酸释放、囊泡转运体表达、树突棘的改变来明确电针调控的内源性物质基础。本研究可为阐明电针的作用机理提供帮助，也为研发以皮层为靶点的PD治疗提供新策略。

Previous results have proved that high frequency electro-acupuncture (EA) stimulation could alleviate motor symptoms in parkinsonian rats. However, the mechanisms of EA on the central nervous systems are unclear. Recent studies suggested that stimulation directly activation of cortical neurons can interfere with the abnormal synchronized oscillation in the cortico-basal ganglia pathway, and therefore can facilitate the improvement of movement disorders.. Our preliminary studies indicated that EA could modulate the discharge of cortical neurons and the release of glutamate. In this study, We hypothesized that EA stimulation, which targeted on the abnormal neuronal activities in the motor cortex , can improve motor symptoms through modulation of the balance between the excitatory/ inhibitory cortical neurons medicated by glutamate, and the modulation of abnormal synchronized oscillation in the cortico-basal ganglia pathway. Deep brain stimulation (DBS) or decortication were used as control, EA stimulation targets in the cortex were confirmed by assessing the influence of EA stimulation on the motor behaviors of rats and electrical activity in cortical neurons. Multiunit array were applied to synchronically record the local field potential and spike in the cortex and the cortico-basal ganglia in order to identify the modulatory approaches of EA stimulation. The release of glutamate, the expression of transporter and spine in the dendrite were tested to identified the modulatory substance within the brain. This research could provide insights for the explanation of EA stimulation mechanism, and contribute to the development of the new therapeutic strategy for PD based on the cortex target.