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Activation of NF-kappa B in Basolateral Amygdala Is Required for Memory Reconsolidation in Auditory Fear Conditioning
Si, Jijian1,2,3; Yang, Jianli2; Xue, Lifen3; Yang, Chenhao1,2,3; Luo, Yixiao3; Shi, Haishui3; Lu, Lin3
刊名PLOS ONE
2012-09-05
DOI10.1371/journal.pone.0043973
7期:9
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
资助者National Science Foundation of China ; Natural Science Foundation of Beijing Municipality ; Science and Technology Foundation of Tianjin Health Bureau ; National Science Foundation of China ; Natural Science Foundation of Beijing Municipality ; Science and Technology Foundation of Tianjin Health Bureau
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]LONG-TERM-MEMORY ; POSTTRAUMATIC-STRESS-DISORDER ; TRANSCRIPTION FACTOR ; SYNAPTIC PLASTICITY ; EXPRESSION ; RETRIEVAL ; ALPHA ; MICE ; CONSOLIDATION ; ACETYLATION
英文摘要

Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, manifested as conditioned fear memory. Previously formed memories that are susceptible to disruption immediately after retrieval undergo a protein synthesis-dependent process to become persistent, termed reconsolidation, a process that is regulated by many distinct molecular mechanisms that control gene expression. Increasing evidence supports the participation of the transcription factor NF-kappa B in the different phases of memory. Here, we demonstrate that inhibition of NF-kappa B in the basolateral amygdala (BLA), but not central nucleus of the amygdala, after memory reactivation impairs the retention of amygdala-dependent auditory fear conditioning (AFC). We used two independent pharmacological strategies to disrupt the reconsolidation of AFC. Bilateral intra-BLA infusion of sulfasalazine, an inhibitor of I kappa B kinase that activates NF-kappa B, and bilateral intra-BLA infusion of SN50, a direct inhibitor of the NF-kappa B DNA-binding complex, immediately after retrieval disrupted the reconsolidation of AFC. We also found that systemic pretreatment with sodium butyrate, a histone deacetylase inhibitor that enhances histone acetylation, in the amygdala rescued the disruption of reconsolidation induced by NF-kappa B inhibition in the BLA. These findings indicate that NF-kappa B activity in the BLA is required for memory reconsolidation in AFC, suggesting that NF-kappa B might be a potential pharmacotherapy target for posttraumatic stress disorder.

语种英语
所属项目编号30870895 ; 7091003 ; 06KR04 ; 09KY02
资助者National Science Foundation of China ; Natural Science Foundation of Beijing Municipality ; Science and Technology Foundation of Tianjin Health Bureau ; National Science Foundation of China ; Natural Science Foundation of Beijing Municipality ; Science and Technology Foundation of Tianjin Health Bureau
WOS记录号WOS:000308463800030
引用统计
被引频次:20[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54253
专题中国药物依赖性研究所
作者单位1.Tianjin Med Univ, Tianjin, Peoples R China
2.Tianjin Mental Hlth Ctr, Tianjin, Peoples R China
3.Peking Univ, Natl Inst Drug Dependence, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Si, Jijian,Yang, Jianli,Xue, Lifen,et al. Activation of NF-kappa B in Basolateral Amygdala Is Required for Memory Reconsolidation in Auditory Fear Conditioning[J]. PLOS ONE,2012,7(9).
APA Si, Jijian.,Yang, Jianli.,Xue, Lifen.,Yang, Chenhao.,Luo, Yixiao.,...&Lu, Lin.(2012).Activation of NF-kappa B in Basolateral Amygdala Is Required for Memory Reconsolidation in Auditory Fear Conditioning.PLOS ONE,7(9).
MLA Si, Jijian,et al."Activation of NF-kappa B in Basolateral Amygdala Is Required for Memory Reconsolidation in Auditory Fear Conditioning".PLOS ONE 7.9(2012).
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