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Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex.

Authors
Lee, YJ; Choi, B; Lee, EH; Choi, KS; Sohn, S
Citation
Neuroscience letters, 392(1-2):27-31, 2006
Journal Title
Neuroscience letters
ISSN
0304-39401872-7972
Abstract
Prolonged stress has been shown to impair brain function and increase vulnerability to neuronal injury. To elucidate the in vivo response of neuronal cells to induced stress, we immobilized mice by binding their legs. Levels of reactive oxygen species (ROS) in the cerebral cortex were increased after stress induction. NADPH oxidase, interleukin-1beta (IL-1beta) and cyclooxygenase 2 mRNA (COX-2) expression levels were upregulated, and Fas levels were also increased. The increased expression of these factors was associated with neuronal death, which was confirmed by TUNEL and NeuN staining. OX42 staining was also evident around the TUNEL-stained lesions. From these findings, it appears that immobilization stress induces neuronal death in the mouse cerebral cortex, a process mediated by NADPH oxidase, IL-1beta, COX-2, ROS and Fas. However, this could be inhibited by pretreating the animals with antioxidants such as ebselen or pyrrolidine dithiocarbamate.
MeSH terms
Analysis of VarianceAnimalsAntigens, CD11b/metabolismAntigens, CD95/geneticsAntigens, CD95/metabolismAntioxidants/therapeutic useAzoles/therapeutic useCell Count/methodsCell Death/drug effectsCell Death/physiologyCerebral Cortex/metabolism*Cerebral Cortex/pathology*Cyclooxygenase 2/geneticsCyclooxygenase 2/metabolismGene Expression Regulation/physiologyImmobilization/methodsImmunohistochemistry/methodsIn Situ Nick-End Labeling/methodsInterleukin-1/geneticsInterleukin-1/metabolismMaleMiceMice, Inbred ICRNADPH Oxidase/geneticsNADPH Oxidase/metabolismOrganoselenium Compounds/therapeutic usePhosphopyruvate Hydratase/metabolismRNA, Messenger/biosynthesisReactive Oxygen Species/metabolism*Reverse Transcriptase Polymerase Chain Reaction/methodsStress, Physiological/drug therapyStress, Physiological/metabolism*Stress, Physiological/pathology*
DOI
10.1016/j.neulet.2005.08.065
PMID
16203091
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
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