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
文献类型：期刊论文
| 作者 | Liu Y1; Zhou QX2; Chen J1; Ling QL1; Cao J2; Chi ZQ1; Lu X[*]2; Liu JG[*]1; Hou YY1; Lu B1 |
| 刊名 | JOURNAL OF NEUROSCIENCE
 |
| 出版日期 | 2012 |
| 卷号 | 32期号:35页码:12005-12017 |
| 通讯作者 | lxu@vip.163.com ; jgliu@mail.shcnc.ac.cn |
| 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. |
| 收录类别 | SCI |
| 资助信息 | This research was supported by grants from the National Basic Research Program,from the Ministry of Science and Technology of China [2009CB522005 (J.-G.L.), 2009CB522006 (J.C.), and 2009CB941302 to (L.X.)], and the Foundation of National Natural Science of China [81130087 (J.-G.L.), 81001424 (Y.-Y. H.), 31100775 (Q.-X.Z.), U1032605 (L.X.), and U1132602 (J.C.)], and the grant from Chinese Academy of Sciences [KSCX2-YW-R-253 (J.-G.L.)] |
| 语种 | 英语 |
| 源URL | [http://159.226.149.26:8080/handle/152453/10814]  |
| 专题 | 昆明动物研究所_学习记忆的分子神经机制 |
| 作者单位 | 1.State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, China 2.Laboratory of Learning and Memory, Kunming Institute of Zoology, The Chinese Academy of Sciences, Kunming 65022, China |
| 推荐引用方式 GB/T 7714 | Liu Y,Zhou QX,Chen J,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 Y.,Zhou QX.,Chen J.,Ling QL.,Cao J.,...&Yu C.(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 Y,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. |
入库方式： OAI收割
来源：昆明动物研究所
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