Actin Polymerization-Dependent Increase in Synaptic Arc/Arg3.1 Expression in the Amygdala Is Crucial for the Expression of Aversive Memory Associated with Drug Withdrawal
Liu, Yao2; Zhou, Qi-Xin1; Hou, Yuan-Yuan2; Lu, Bin2; Yu, Chuan2; Chen, Jie2; Ling, Qing-Lan2; Cao, Jun1; Chi, Zhi-Qiang2; Xu, Lin1
刊名JOURNAL OF NEUROSCIENCE
2012-08-29
卷号32期号:35页码:12005-12017
ISSN号0270-6474
DOI10.1523/JNEUROSCI.0871-12.2012
文献子类Article
英文摘要Aversive memories associated with drug withdrawal may contribute to persistent drug seeking. Molecular mechanisms that are critical for aversive memory formation have yet to be elucidated. Recently, we showed in a rat conditioned place aversion (CPA) model that synaptic actin polymerization in the amygdala were required for aversive memory information. Here, we demonstrated that actin polymerization within the amygdala triggered transportation of activity-regulated cytoskeletal-associated protein (Arc/Arg3.1) into amygdalar synapses. Increased synaptic Arc/Arg3.1 expression contributed to aversive memory formation by regulating synaptic AMPA receptor (AMPAR) endocytosis, as in vivo knockdown of amygdalar Arc/Arg3.1 with Arc/Arg3.1-shRNA prevented both AMPAR endocytosis and CPA formation. We also demonstrated that conditioned morphine withdrawal led to induction of LTD in the amygdala through AMPAR endocytosis. We further demonstrated that Arc/Arg3.1-regulated AMPAR endocytosis was GluR2 dependent, as intra-amygdala injection of Tat-GluR2(3Y), a GluR2-derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and aversive memory formation. Therefore, this study extends previous studies on the role of actin polymerization in synaptic plasticity and memory formation by revealing the critical molecular events involved in aversive memory formation as well as LTD induction, and by showing that Arc/Arg3.1 is a crucial mediator for actin polymerization functions, and, thus, underscores the unknown details of how actin polymerization mediates synaptic plasticity and memory.
资助项目National Basic Research Program[00000000] ; Ministry of Science and Technology of China[2009CB522005] ; Ministry of Science and Technology of China[2009CB522006] ; Ministry of Science and Technology of China[2009CB941302] ; Foundation of National Natural Science of China[81130087] ; Foundation of National Natural Science of China[81001424] ; Foundation of National Natural Science of China[31100775] ; Foundation of National Natural Science of China[U1032605] ; Foundation of National Natural Science of China[U1132602] ; Chinese Academy of Sciences[KSCX2-YW-R-253]
WOS关键词AMPA RECEPTOR TRAFFICKING ; LONG-TERM POTENTIATION ; BEHAVIORAL SENSITIZATION ; NUCLEUS-ACCUMBENS ; HIPPOCAMPAL-NEURONS ; LATERAL AMYGDALA ; DENDRITIC SPINES ; PLACE AVERSION ; MESSENGER-RNA ; IN-VIVO
WOS研究方向Neurosciences & Neurology
语种英语
出版者SOC NEUROSCIENCE
WOS记录号WOS:000308213900009
内容类型期刊论文
源URL[http://119.78.100.183/handle/2S10ELR8/277983]  
专题药理学第二研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Liu, Jing-Gen
作者单位1.Chinese Acad Sci, Kunming Inst Zool, Lab Learning & Memory, Kunming 65022, Peoples R China
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China;
推荐引用方式
GB/T 7714
Liu, Yao,Zhou, Qi-Xin,Hou, Yuan-Yuan,et al. Actin Polymerization-Dependent Increase in Synaptic Arc/Arg3.1 Expression in the Amygdala Is Crucial for the Expression of Aversive Memory Associated with Drug Withdrawal[J]. JOURNAL OF NEUROSCIENCE,2012,32(35):12005-12017.
APA Liu, Yao.,Zhou, Qi-Xin.,Hou, Yuan-Yuan.,Lu, Bin.,Yu, Chuan.,...&Liu, Jing-Gen.(2012).Actin Polymerization-Dependent Increase in Synaptic Arc/Arg3.1 Expression in the Amygdala Is Crucial for the Expression of Aversive Memory Associated with Drug Withdrawal.JOURNAL OF NEUROSCIENCE,32(35),12005-12017.
MLA Liu, Yao,et al."Actin Polymerization-Dependent Increase in Synaptic Arc/Arg3.1 Expression in the Amygdala Is Crucial for the Expression of Aversive Memory Associated with Drug Withdrawal".JOURNAL OF NEUROSCIENCE 32.35(2012):12005-12017.
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