Xu Xiangping, Sun Ruopeng, Jin Ruifeng
Department of Pediatrics, Qilu Hospital of Shandong University, Jinan 250012, China.
Epilepsy Behav. 2008 Oct;13(3):445-8. doi: 10.1016/j.yebeh.2008.05.020. Epub 2008 Jul 7.
Treatment with the ketogenic diet has been used to control refractory epilepsy for many years, although its anticonvulsant mechanism is unknown. By modulating synaptic transmission in the hippocampus, kainate receptors and their RNA editing might play a role in the antiseizure action of the treatment. To investigate the potential effect of the ketogenic diet on GluR(5) mRNA and GluR(6) mRNA expression and Q/R site editing, we used the kainate-induced epilepsy model in the present study. Reverse transcription polymerase chain reaction was performed to determine GluR(5) and GluR(6) mRNA expression, and RNA editing was analyzed with the BbvIota restriction enzyme assay. The results demonstrated that expression of GluR(6) mRNA, but not GluR(5) mRNA, was significantly increased after 8 weeks of dietary treatment. Neither the GluR(5) nor the GluR(6) RNA editing rate at the Q/R site was significantly changed by dietary treatment. These data indicate that GluR(6) may be involved in the anticonvulsant mechanism of ketogenic diet treatment.
生酮饮食疗法已被用于控制难治性癫痫多年，尽管其抗惊厥机制尚不清楚。通过调节海马体中的突触传递，海人酸受体及其RNA编辑可能在该治疗的抗癫痫作用中发挥作用。为了研究生酮饮食对GluR(5) mRNA和GluR(6) mRNA表达以及Q/R位点编辑的潜在影响，我们在本研究中使用了海人酸诱导的癫痫模型。进行逆转录聚合酶链反应以确定GluR(5)和GluR(6) mRNA表达，并使用BbvIota限制性内切酶分析法分析RNA编辑。结果表明，饮食治疗8周后，GluR(6) mRNA的表达显著增加，而GluR(5) mRNA的表达未显著增加。饮食治疗对Q/R位点的GluR(5)和GluR(6) RNA编辑率均无显著影响。这些数据表明，GluR(6)可能参与生酮饮食治疗的抗惊厥机制。
