Suppr超能文献

5-羟色胺1A受体介导对大鼠纹状体中乙醇诱导的抗坏血酸释放的抑制作用(通过微透析法研究)。

5-HT1A receptors mediate inhibition of ethanol-induced ascorbic acid release in rat striatum studied by microdialysis.

作者信息

Wu C F, Liu J, Consolo S, Liu W

机构信息

Department of Pharmacology of Chinese Materia Medica, Shenyang Pharmaceutical University, China.

出版信息

Neurosci Lett. 1998 Jul 3;250(2):95-8. doi: 10.1016/s0304-3940(98)00436-4.

Abstract

Our previous study showed that the serotonergic system was involved in the ethanol-induced striatal ascorbic acid release in rat. In the present study, the 5-HT1A agonists and antagonists were used to analyze the possible mechanism of ethanol-induced ascorbic acid release in rat striatum. The results showed that ethanol (3.0 g/kg, i.p.) significantly increased striatal ascorbic acid release. Buspirone (5.0 mg/kg, s.c.), a partial agonist of 5-HT1A receptors, and 8-OH-DPAT (0.5 mg/kg, s.c.), a selective agonist of 5-HT1A receptors, showed no effect on basal ascorbic acid release in striatum, but both drugs significantly antagonized the ascorbic acid release induced by ethanol in striatum. WAY 100635 (0.5 mg/kg, s.c.), a selective antagonist of 5-HT1A receptors, affecting neither the basal nor the ethanol-induced ascorbic acid release per se, antagonized the suppressing effect of 8-OH-DPAT on ethanol-induced ascorbic acid release in striatum. This study gives the first evidence that activation of 5-HT1A receptors is involved in ethanol-induced ascorbic acid release in rat striatum.

摘要

我们之前的研究表明,血清素能系统参与了乙醇诱导的大鼠纹状体抗坏血酸释放。在本研究中,使用5-HT1A激动剂和拮抗剂来分析乙醇诱导大鼠纹状体抗坏血酸释放的可能机制。结果表明,乙醇(3.0克/千克,腹腔注射)显著增加纹状体抗坏血酸释放。丁螺环酮(5.0毫克/千克,皮下注射),一种5-HT1A受体的部分激动剂,以及8-OH-DPAT(0.5毫克/千克,皮下注射),一种5-HT1A受体的选择性激动剂,对纹状体基础抗坏血酸释放无影响,但两种药物均显著拮抗乙醇诱导的纹状体抗坏血酸释放。WAY 100635(0.5毫克/千克,皮下注射),一种5-HT1A受体的选择性拮抗剂,本身既不影响基础抗坏血酸释放也不影响乙醇诱导的抗坏血酸释放,拮抗了8-OH-DPAT对乙醇诱导的纹状体抗坏血酸释放的抑制作用。本研究首次证明5-HT1A受体的激活参与了乙醇诱导的大鼠纹状体抗坏血酸释放。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验