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电针减少幼鼠海人酸诱导的癫痫持续状态中的癫痫发作活动并增强GAD 67和谷氨酸转运体表达。

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

作者信息

Vega-García Angelica, Neri-Gómez Teresa, Buzoianu-Anguiano Vinnitsa, Guerra-Araiza Christian, Segura-Uribe Julia, Feria-Romero Iris, Orozco-Suarez Sandra

机构信息

Unidad de Investigación Médica en Enfermedades Neurológicas, Hospital de Especialidades "Dr. Bernardo Sepúlveda", Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México CP.06720, Mexico.

Laboratorio de Nanomateriales, Centro de Investigación en Ciencias de la Salud, Universidad Autónoma de San Luis Potosí, Estado de San Luis Potosí CP.78210, Mexico.

出版信息

Behav Sci (Basel). 2019 Jun 27;9(7):68. doi: 10.3390/bs9070068.

Abstract

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.

摘要

癫痫持续状态(SE)是小儿神经病学中最严重的并发症之一。临床研究表明,电针(EA)作为一种治疗方法,在控制部分性癫痫发作和继发性全身性阵挛性癫痫发作方面具有积极作用。电针可促进γ-氨基丁酸(GABA)和一些阿片类物质等神经递质的释放。本研究旨在评估水沟穴(SG_DM26)穴位电刺激对早期癫痫持续状态模型中谷氨酸脱羧酶67(GAD67)和谷氨酸转运体EAAC1表达的抗惊厥和神经调节作用。在出生后第10天(10-PD),将体重22-26 g的雄性大鼠分为16组,包括对照组和治疗组:单纯刺激组、电刺激组、抗惊厥药物治疗组以及联合治疗组——电刺激与戊巴比妥(PB)联合治疗组。采用 kainic acid(KA)诱导癫痫持续状态,并测量以下参数:运动行为以及GAD67和EAAC1的表达。结果表明水沟穴电针具有抗癫痫作用。其可能的机制很可能是抑制性神经递质GABA的产生增加,这表现为GAD67和EAAC1表达的增加,以及电针和戊巴比妥的神经调节作用之间的潜在协同作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/298a/6680393/1f8ff2fc68f5/behavsci-09-00068-g001.jpg

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