...
首页> 外文期刊>Behavioral Sciences >Electroacupuncture Reduces Seizure Activity and Enhances GAD 67 and Glutamate Transporter Expression in Kainic Acid Induced Status Epilepticus in Infant Rats
【24h】

Electroacupuncture Reduces Seizure Activity and Enhances GAD 67 and Glutamate Transporter Expression in Kainic Acid Induced Status Epilepticus in Infant Rats

机译:电针减少癫痫发作活性,并在幼儿大鼠中吞噬117和谷氨酸转运蛋白表达和谷氨酸诱导状态癫痫患者

获取原文
           

摘要

Status epilepticus (SE) is one of the most significant complications in pediatric neurology. Clinical studies have shown positive effects of electroacupuncture (EA) as a therapeutic alternative in the control of partial seizures and secondary generalized clonic seizures. EA promotes the release of neurotransmitters such as GABA and some opioids. The present study aimed to evaluate the anticonvulsive and neuromodulatory effects of Shui Gou DM26 (SG_DM26) acupuncture point electrostimulation on the expression of the glutamate decarboxylase 67 (GAD67) enzyme and the glutamate transporter EAAC1 in an early SE model. At ten postnatal days (10-PD), male rats weighing 22–26 g were divided into 16 groups, including control and treatment groups: Simple stimulation, electrostimulation, anticonvulsant drug treatment, and combined treatment—electrostimulation and pentobarbital (PB). SE was induced with kainic acid (KA), and the following parameters were measured: Motor behavior, and expression of GAD67 and EAAC1. The results suggest an antiepileptic effect derived from SG DM26 point EA. The possible mechanism is most likely the increased production of the inhibitory neurotransmitter GABA, which is observed as an increase in the expression of both GAD67 and EAAC1, as well as the potential synergy between the neuromodulator effects of EA and PB.
机译:状态癫痫(SE)是儿科神经内科最重要的并发症之一。临床研究表明了电针(EA)作为治疗替代的局部癫痫发作和二次广义克隆癫痫发作的含量替代的正效应。 EA促进释放神经递质,如GABA和一些阿片类药物。本研究旨在评估水GOU DM26(SG_DM26)针灸点电刺激对早期SE模型中谷氨酸脱羧酶67(GAD67)酶和谷氨酸转运蛋白eac1的表达的抗抑化和神经调节作用。在十天(10-PD)(10-PD),称重22-26g的雄性大鼠分为16组,包括控制和治疗组:简单的刺激,静电,抗惊厥药物治疗,以及组合治疗 - 电刺激和戊巴比妥(PB)。用Kainic酸(Ka)诱导Se,测量以下参数:电机行为,以及GAD67和EAAC1的表达。结果表明衍生自SG DM26点EA的抗癫痫效果。可能的机制最有可能增加抑制性神经递质GABA的增加,这被观察到GAD67和EAAC1表达的增加,以及EA和Pb的神经调节器效应之间的潜在协同作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号