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电刺激和损毁大鼠丘脑前核对抗 kainic 酸诱导的局灶性边缘叶癫痫的抗惊厥作用。

Anti-convulsant effect of electrical stimulation and lesioning of the anterior thalamic nucleus on kainic acid-induced focal limbic seizure in rats.

作者信息

Takebayashi Seiji, Hashizume Kiyotaka, Tanaka Tatsuya, Hodozuka Akira

机构信息

Department of Neurosurgery, Asahikawa Medical College, 2-1 Midorigaoka-Higashi, Asahikawa 078-8510, Japan.

出版信息

Epilepsy Res. 2007 May;74(2-3):163-70. doi: 10.1016/j.eplepsyres.2007.03.007. Epub 2007 Apr 19.

DOI:10.1016/j.eplepsyres.2007.03.007
PMID:17448643
Abstract

PURPOSE

We examined the effect of electrical stimulation and lesioning of the anterior nucleus of the thalamus (ANT) on focal limbic seizures induced by intraamygdaloid kainic acid (KA) injection in a rat model. To address the mechanism underlying these anti-convulsant actions, cerebral glucose metabolism following ANT electrical stimulation and lesioning was also assessed.

METHODS

Wistar rats were divided into five major groups: control, unilateral and bilateral ANT electrical stimulation, and unilateral and bilateral ANT lesioning. After KA injection, average clinical-seizure frequencies in each group were measured. Local cerebral glucose utilization (LCGU) was also measured using [(14)C] 2-deoxyglucose autoradiography in three groups: control, ANT electrical stimulation and ANT lesioning.

RESULTS

Animals subjected to ANT electrical stimulation and lesioning exhibited significantly decreased mean seizure frequency and secondary generalized seizure frequency, compared with control-animals. In control-group, LCGU was markedly increased at both the limbic and corticothalamic circuits sites. While in ANT stimulation or lesioning-group, there was significant reduction in LCGU at the corticothalamic circuit sites, but not so considerable decrease at the limbic structures.

CONCLUSION

ANT electrical stimulation and lesioning in the focal limbic seizure model were effective on convulsive seizures and secondary generalization, specifically with respect to the severity of these seizures.

摘要

目的

我们在大鼠模型中研究了丘脑前核(ANT)的电刺激和毁损对杏仁核内注射 kainic 酸(KA)诱发的局灶性边缘叶癫痫发作的影响。为了探究这些抗惊厥作用的潜在机制,还评估了 ANT 电刺激和毁损后的脑葡萄糖代谢情况。

方法

将 Wistar 大鼠分为五大组:对照组、单侧和双侧 ANT 电刺激组以及单侧和双侧 ANT 毁损组。注射 KA 后,测量每组的平均临床癫痫发作频率。还使用[(14)C]2 - 脱氧葡萄糖放射自显影术在三组中测量局部脑葡萄糖利用(LCGU):对照组、ANT 电刺激组和 ANT 毁损组。

结果

与对照动物相比,接受 ANT 电刺激和毁损的动物平均癫痫发作频率和继发性全身性癫痫发作频率显著降低。在对照组中,边缘叶和皮质丘脑回路部位的 LCGU 均显著增加。而在 ANT 刺激或毁损组中,皮质丘脑回路部位的 LCGU 显著降低,但边缘叶结构处的降低幅度不那么明显。

结论

在局灶性边缘叶癫痫模型中,ANT 电刺激和毁损对惊厥性发作和继发性全身性发作有效,特别是在这些发作的严重程度方面。

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