5-Hydroxytryptamine attenuates free radical injury in primary mouse cortical cultures

被引：9

作者：

Kang, JY

Kang, HJ

Chung, YK

Gwag, BJ

Noh, JS ^{[1
]}

机构：

[1] Ajou Univ, Sch Med, Dept Psychiat & Behav Sci, Suwon 442749, Kyungkido, South Korea

[2] Ajou Univ, Sch Med, Dept Pharmacol, Suwon 442749, Kyungkido, South Korea

[3] Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 442749, Kyungkido, South Korea

来源：

NEUROREPORT | 2001年 / 12卷 / 05期

关键词：

aapoptosis; cortical cultures; free radicals; 5-hydroxytryptamine; necrosis;

D O I：

10.1097/00001756-200104170-00020

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The effects of 5-hydroxytryptamine (5-HT) on several types of neuronal injury in mouse cortical cell cultures were tested. Co-treatment with 5-HT prevented free radical-mediated neuronal necrosis induced by FeCl2 or buthionine sulfoximine (BSO) in a dose-dependent manner. Subtype antagonists did not reverse the protective effect and 5-HT showed direct free radical scavenging activity evidenced by its ability to reduce the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) in a cell-free system. Excitotoxic necrosis induced by NMDA or apoptosis induced by staurosporine was not sensitive to 5-HT treatment. These features raise the possibility that the endogenous neurotransmitter 5-HT may work as an innate antioxidant defense mechanism in the CNS. NeuroReport 12:963-966 (C) 2001 Lippincott Williams & Wilkins.

引用

页码：963 / 966

页数：4

共 23 条

[1] S-100β protects cultured neurons against glutamate- and staurosporine-induced damage and is involved in the antiapoptotic action of the 5 HT1A-receptor agonist, Bay x 3702 [J].