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毛果芸香碱诱导的大鼠癫痫持续状态:海马、纹状体和额叶皮质中的脂质过氧化水平、亚硝酸盐形成、γ-氨基丁酸能和谷氨酸能受体改变

Pilocarpine-induced status epilepticus in rats: lipid peroxidation level, nitrite formation, GABAergic and glutamatergic receptor alterations in the hippocampus, striatum and frontal cortex.

作者信息

Freitas R M, Sousa F C F, Vasconcelos S M M, Viana G S B, Fonteles M M F

机构信息

Department of Physiology and Pharmacology, Laboratory of Neuropharmacology, School of Medicine, Federal University of Ceará, Rua Frederico Severo 201, Ap 103, Bl 07, Messejana, Fortaleza 60830-310, Brazil.

出版信息

Pharmacol Biochem Behav. 2004 Jun;78(2):327-32. doi: 10.1016/j.pbb.2004.04.004.

Abstract

The aim of the study was to investigate the lipid peroxidation levels, nitrite formation, GABAergic and glutamatergic receptor densities in the hippocampus, frontal cortex and striatum of Wistar rats after seizures and status epilepticus (SE) induced by pilocarpine. The control group was treated with 0.9% saline and sacrificed 1 h after the treatment. One group of rats was administered with pilocarpine (400 mg/kg sc) and sacrificed 1 h after treatment. The result shows that pilocarpine administration and the resulting SE produced a significant increase of lipid peroxidation level in the hippocampus (46%), striatum (25%) and frontal cortex (21%). In nitrite formation, increases of 49%, 49% and 75% in hippocampus, striatum and frontal cortex, respectively, was observed. Pilocarpine treatment induced down-regulation of GABAergic receptors in the hippocampus (38%), striatum (15%) and frontal cortex (11%). However, with regard to glutamatergic receptor densities, increases in the hippocampus (11%), striatum (17%) and frontal cortex (14%) was observed during the observation period. These results show a direct evidence of lipid peroxidation and nitrite formation during seizure activity that could be responsible for the GABAergic and glutamatergic receptor concentration changes during the establishment of SE induced by pilocarpine.

摘要

本研究旨在调查匹鲁卡品诱导癫痫发作和癫痫持续状态(SE)后,Wistar大鼠海马、额叶皮质和纹状体中的脂质过氧化水平、亚硝酸盐形成、GABA能和谷氨酸能受体密度。对照组用0.9%生理盐水处理,并在处理后1小时处死。一组大鼠给予匹鲁卡品(400mg/kg皮下注射),并在处理后1小时处死。结果显示,给予匹鲁卡品及由此产生的SE导致海马(46%)、纹状体(25%)和额叶皮质(21%)的脂质过氧化水平显著增加。在亚硝酸盐形成方面,分别观察到海马、纹状体和额叶皮质增加了49%、49%和75%。匹鲁卡品处理导致海马(38%)、纹状体(15%)和额叶皮质(11%)的GABA能受体下调。然而,关于谷氨酸能受体密度,在观察期内观察到海马(11%)、纹状体(17%)和额叶皮质(14%)增加。这些结果直接证明了癫痫发作活动期间脂质过氧化和亚硝酸盐形成,这可能是匹鲁卡品诱导的SE建立过程中GABA能和谷氨酸能受体浓度变化的原因。

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