Du Jing, Sun Zuo-Li, Jia Jun, Wang Xuan, Wang Xiao-Min
Department of Physiology, Capital Medical University, Beijing 100069, China.
Sheng Li Xue Bao. 2011 Aug 25;63(4):305-10.
The purpose of the present study is to observe the effect of electro-acupuncture (EA) stimulation on intracerebral neurotransmitters in a rat model of Parkinson's disease (PD), and explore the possible mechanism. We used 6-hydroxydopamine (6-OHDA) injection in medial forebrain bundle (MFB) in the right brain of Sprague Dawley (SD) rat to establish the parkinsonian rat model, and randomly divided the PD rats into model and 100 Hz EA stimulation groups (n =10 in each group). EA stimulation group received 4 courses of EA stimulation on Baihui (GV-20) and Dazhui (GV-14) acupuncture points. Moreover, ten rats were randomly selected as sham operation group, only receiving normal saline (NS) injection in MFB. Then apomorphine (APO)-induced rotational behavior in different groups was recorded, and the contents of γ-aminobutyric acid (GABA) in the brain were analyzed with high pressure/performance liquid chromatography-electrochemical detection (HPLC-ECD). The results showed that model group exhibited abnormal rotational behavior with APO treatment, suggesting the successful establishment of PD model. Compared with sham operation group, model group showed increased GABA contents in cortex and striatum, as well as decreased GABA content in ventral midbrain, on the lesioned side. EA stimulation could effectively ameliorate the abnormal rotational behavior of PD rat. Compared with the model group, EA stimulation decreased the ratio of GABA content on the lesioned side to that on unlesioned side in the cortex, while increased the ratios in the striatum and cerebellum. However, there was no difference of the ratio in the ventral midbrain among three groups. These results suggest high-frequency EA stimulation significantly improves the abnormal behavior of PD rats, which may exert through enhancing the inhibitory effect of cerebellum-basal ganglia-cortical loop on motor center.
本研究旨在观察电针刺激对帕金森病(PD)大鼠模型脑内神经递质的影响,并探讨其可能机制。我们通过向Sprague Dawley(SD)大鼠右侧脑内侧前脑束(MFB)注射6-羟基多巴胺(6-OHDA)建立帕金森病大鼠模型,并将PD大鼠随机分为模型组和100 Hz电针刺激组(每组n = 10)。电针刺激组在百会(GV-20)和大椎(GV-14)穴位接受4个疗程的电针刺激。此外,随机选取10只大鼠作为假手术组,仅在MFB注射生理盐水(NS)。然后记录不同组阿扑吗啡(APO)诱导的旋转行为,并用高压/高效液相色谱-电化学检测(HPLC-ECD)分析脑内γ-氨基丁酸(GABA)含量。结果显示,模型组经APO处理后出现异常旋转行为,提示PD模型建立成功。与假手术组相比,模型组损伤侧皮质和纹状体GABA含量增加,腹侧中脑GABA含量降低。电针刺激可有效改善PD大鼠的异常旋转行为。与模型组相比,电针刺激降低了损伤侧与未损伤侧皮质GABA含量的比值,而增加了纹状体和小脑的比值。然而,三组腹侧中脑的比值无差异。这些结果表明,高频电针刺激可显著改善PD大鼠的异常行为,其机制可能是通过增强小脑-基底神经节-皮质环路对运动中枢的抑制作用。