Jin Hong-Bing, Li Bing, Gu Jing, Cheng Jie-Shi, Yang Ru
National Key Laboratory of Medical Neurobiology, Shanghai Medical College of Fudan University, Shanghai 200032, P R China.
Acupunct Electrother Res. 2005;30(3-4):207-17. doi: 10.3727/036012905815901280.
Electro-acupuncture (EA) partially inhibited epilepsy with great success. The biological basis underlying EA anti-convulsion remained uncertain, which resulted in limited application and slow improvement of acupuncture. Our previous study indicated that taurine may play an inhibitory role against epilepsy as an inhibitory amino acid in the central nervous system and EA may inhibit epilepsy via up-regulating the expression of taurine transporter to increase the release of taurine. Involvement of taurine in kainic acid (KA)-induced epilepsy and anti-convulsion of EA was further addressed on taurine deficiency animal in the present work. We instituted endogenous taurine-deficiency model by supplementation of beta-alanine (3%) in drinking water for continuous 10 days initially, injected KA into lateral cerebral ventricle to induce epileptic seizure, and performed EA treatment on DU26 "RenZhong" and K "YongQuan" acupoints by an EA apparatus (Model G6805-2) using successive waves with the frequency 64Hz and the current intensity 0.8-1.0 mA for 30 minutes in Sprague-Dawley (SD) rats. Taurine levels markedly decreased in cortex, hippocampus, striatum and cerebellum of rats after beta-alanine administration by fluore-HPLC measurement. EA alleviated epileptic activity in rats at 3.5 h time point after KA injection, whereas beta-alanine-induced taurine depletion rendered rats more susceptible to KA-induced epilepsy. Taurine transporter level increased after EA treatment. These results suggested that taurine participated in epileptogenesis and EA may be related to taurine in controlling epileptic seizure.
电针(EA)在抑制癫痫方面取得了一定成功。电针抗惊厥的生物学基础仍不明确,这导致针刺疗法的应用受限且进展缓慢。我们之前的研究表明,牛磺酸作为中枢神经系统中的一种抑制性氨基酸,可能对癫痫发挥抑制作用,并且电针可能通过上调牛磺酸转运体的表达来增加牛磺酸的释放从而抑制癫痫。在本研究中,我们在牛磺酸缺乏的动物模型上进一步探讨了牛磺酸在 kainic 酸(KA)诱导的癫痫及电针抗惊厥中的作用。我们首先通过在饮水中补充β-丙氨酸(3%)持续 10 天建立内源性牛磺酸缺乏模型,然后向大鼠侧脑室注射 KA 诱导癫痫发作,并使用 G6805 - 2 型电针仪对 SD 大鼠的督脉 26 穴“人中”和肾经“涌泉”穴进行电针治疗,采用连续波,频率 64Hz,电流强度 0.8 - 1.0mA,持续 30 分钟。通过荧光高效液相色谱法测量发现,给予β-丙氨酸后大鼠皮质、海马、纹状体和小脑的牛磺酸水平显著降低。在注射 KA 后 3.5 小时,电针减轻了大鼠的癫痫活动,而β-丙氨酸诱导的牛磺酸耗竭使大鼠对 KA 诱导的癫痫更敏感。电针治疗后牛磺酸转运体水平升高。这些结果表明,牛磺酸参与癫痫发生过程,电针在控制癫痫发作方面可能与牛磺酸有关。