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

Authors
Kang, JY; Kang, HJ; Chung, YK; Gwag, BJ; Noh, JS
Citation
Neuroreport, 12(5):963-966, 2001
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
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.
MeSH terms
AnimalsAntioxidants/pharmacology*Apoptosis/drug effectsCell Death/drug effectsCells, CulturedCerebral Cortex/pathology*Free Radical Scavengers/pharmacologyFree Radicals/toxicity*MiceNeurons/drug effects*Neuroprotective Agents/pharmacologySerotonin/pharmacology*Serotonin Antagonists/pharmacologyStaurosporine/toxicity
PMID
11303769
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > School of Medicine / Graduate School of Medicine > Psychiatry & Behavioural Sciences
AJOU Authors
강, 지윤정, 영기곽, 병주노, 재성
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