Shi Hong, Li Jiang-hui, Ji Chang-fu, Shang Hong-yan, Qiu En-chao, Wang Jing-jing, Jing Xiang-hong
Institute of Acu-mo.ribustion, China Academy of Chinese Medical Sciences, Beijing 100700, China.
Zhen Ci Yan Jiu. 2010 Feb;35(1):17-21.
To observe the effect of electroacupuncture (EA) on cortical spreading depression (CSD) and contents of plasma calcitonin gene-related peptide (CGRP) and substance P (SP) in migraine rats.
Thirty male SD rats were equally randomized into control, model and EA groups. Migraine model was established by topical application of KCI (3 mol/L) immersed in a piece of filter paper to the cerebral cortex (parietal lobe, 6 mm posterior to the Bregma and 5 mm to the sagital fissure) after exposure of the skull (in reference to Michael' method). KCI stimulation evoked CSD potentials (3 mm rostral to the Bregma, and 2 mm to the sagital fissure) were recorded by using a glass microelectrode. For rats of control group, filter paper containing 0.9% NaCl was applied to the same parietal cortex area. EA (1 mA, 2 Hz/100 Hz) was applied to bilateral "Yanglingquan" (GB 34) and "Taichong" (LR 3) for 30 min. The contents of plasma CGRP and SP were assayed by radioimmunoassay.
CSD was induced 3-5 min after application of KCI to the parietal lobe. The average amplitude of model group was (-25.13 +/- 1.23) mV, and that of EA group was (-19.19 +/- 1.53) mV, displaying a significant reduction of CSD amplitude after EA (P < 0.01). Comparison among 3 groups showed that both plasma CGRP and SP contents in model group were significantly higher than those of control group (P < 0.001, P < 0.01), while compared with model group, plasma CGRP and SP levels in EA group decreased considerably (P < 0.05, P < 0.001), suggesting an inhibitory effect of EA on pain-producing substance.
EA of GB 34 and LR 3 can effectively suppress KCI provoked cortical spreading depression and plasma CGRP and SP levels in the rat, which may contribute to its effect in relieving migraine in clinic.
观察电针（EA）对偏头痛大鼠皮层扩散性抑制（CSD）及血浆降钙素基因相关肽（CGRP）和P物质（SP）含量的影响。
将30只雄性SD大鼠随机分为对照组、模型组和电针组，每组10只。参照Michael法，暴露颅骨后，将浸有3 mol/L氯化钾（KCI）的滤纸贴于大脑皮层（顶叶，前囟后6 mm，矢状缝旁5 mm）建立偏头痛模型。用玻璃微电极记录KCI刺激诱发的CSD电位（前囟前方3 mm，矢状缝旁2 mm）。对照组大鼠在相同顶叶皮层区域贴含0.9%氯化钠的滤纸。电针双侧“阳陵泉”（GB 34）和“太冲”（LR 3），强度1 mA，频率2 Hz/100 Hz，持续30分钟。采用放射免疫分析法检测血浆CGRP和SP含量。
向顶叶应用KCI后3 - 5分钟诱发CSD。模型组平均波幅为（-25.13±1.23）mV，电针组为（-19.19±1.53）mV，电针后CSD波幅显著降低（P < 0.01）。三组比较，模型组血浆CGRP和SP含量均显著高于对照组（P < 0.001，P < 0.01），而电针组与模型组比较，血浆CGRP和SP水平明显降低（P < 0.05，P < 0.001），提示电针对致痛物质有抑制作用。
电针GB 34和LR 3能有效抑制KCI诱发的大鼠皮层扩散性抑制及血浆CGRP和SP水平，这可能是其临床缓解偏头痛的作用机制。
