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Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation
Tang, Ming-ming1,2; Lin, Wen-juan1,2,3; Zhang, Jun-tao1,2; Zhao, Ya-wei1,2; Li, Ying-cong1
2017-11-01
发表期刊BRAIN BEHAVIOR AND IMMUNITY
ISSN0889-1591
文章类型Article
卷号66期号:0页码:322-331
摘要

Our previous work demonstrated that neuroinflammation evoked by triple repeated central LPS challenges inhibited adult hippocampal neurogenesis that were correlated with the depressive-like behavioral symptoms induced by neuroinflammation. These findings suggest that hippocampal neurogenesis might be one of biological mechanisms underlying depression induced by neuroinflammation and targeting neurogenesis might lead to new therapeutic strategies for the treatment of depression. In this study, we manipulated adult hippocampal neurogenesis using fibroblast growth factor 2 (FGF2), one crucial molecule modulating cell proliferation and survival in central nervous system, and investigate the involvement and the potential therapeutic effects of FGF2 on neuroinflammation-induced depression. Central lipopolysaccharides (LPS) challenges were used as previously to evoke the neuroinflammatory state in the brain of rat. Exogenous FGF2 was infused into lateral ventricle during the neuroinflammatory state. It was found that the protein expression of FGF2 in hippocampus was inhibited by neuroinflammation. The activation of extracellular signal-regulated kinase (ERR), the downstream molecule of FGF2, was also inhibited by neuroinflammation. Exogenous FGF2 infusions prevented the decrease in phosphorylation of ERK1/2 under neuroinflammation state. Exogenous FGF2 reversed depressive-like behaviors and the impaired hippocampal neurogenesis induced by neuroinflammation. These findings provide evidence that the FGF2-ERK1/2 pathway is involved in the pathophysiology of depressive-like behaviors, and manipulating the neurogenesis pathway is a viable therapeutic approach to inflammation-associated depression. (C) 2017 Elsevier Inc. All rights reserved.

关键词Neuroinflammation Depressive-like behavior Neurogenesis Fibroblast growth factor 2 Extracellular signal-regulated kinase 1/2
DOI10.1016/j.bbi.2017.05.013
收录类别SCI
语种英语
项目资助者National Natural Science Foundation of China(31170987 ; CAS Key Laboratory of Mental Health, Institute of Psychology(KLMH20142G01) ; 31440045)
WOS研究方向Immunology ; Neurosciences & Neurology
WOS类目Immunology ; Neurosciences
WOS记录号WOS:000414236600031
WOS标题词Science & Technology ; Life Sciences & Biomedicine
关键词[WOS]FIBROBLAST-GROWTH-FACTOR ; ADULT-RAT BRAIN ; FORCED SWIM STRESS ; CELL-PROLIFERATION ; SUBVENTRICULAR ZONE ; MAJOR DEPRESSION ; INTERFERON-GAMMA ; MESSENGER-RNA ; DENTATE GYRUS ; FACTOR SYSTEM
引用统计
被引频次:6[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/22014
专题中国科学院心理健康重点实验室
作者单位1.Inst Psychol, CAS Key Lab Mental Hlth, Beijing 100101, Peoples R China
2.Univ Chinese Acad Sci, Beijing, Peoples R China
3.Chinese Acad Sci, Inst Psychol, Brain Behav Res Ctr, Beijing 100101, Peoples R China
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Tang, Ming-ming,Lin, Wen-juan,Zhang, Jun-tao,et al. Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation[J]. BRAIN BEHAVIOR AND IMMUNITY,2017,66(0):322-331.
APA Tang, Ming-ming,Lin, Wen-juan,Zhang, Jun-tao,Zhao, Ya-wei,&Li, Ying-cong.(2017).Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation.BRAIN BEHAVIOR AND IMMUNITY,66(0),322-331.
MLA Tang, Ming-ming,et al."Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation".BRAIN BEHAVIOR AND IMMUNITY 66.0(2017):322-331.
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