Inverse Synaptic Tagging of Inactive Synapses via Dynamic Interaction of Arc/Arg3.1 with CaMKII尾

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• 作者：Hiroyuki Okuno¹ ; ⁶ ; ^{okuno@m.u-tokyo.ac.jp} ; Kaori Akashi³ ; Yuichiro Ishii¹ ; ² ; Nan Yagishita-Kyo¹ ; ² ; Kanzo Suzuki¹ ; ² ; Mio Nonaka¹ ; ² ; ⁶ ; Takashi Kawashima¹ ; ² ; Hajime Fujii¹ ; ⁶ ; Sayaka Takemoto-Kimura¹ ; ⁴ ; Manabu Abe³ ; Rie Natsume³ ; Shoaib Chowdhury⁵ ; Kenji Sakimura³ ; ⁶ ; Paul  ; F. Worley⁵ ; Haruhiko Bito¹ ; ² ; ⁶ ; ^{hbito@m.u-tokyo.ac.jp}
• 刊名：Cell
• 出版年：2012
• 期刊代码：50_00928674
• 类别：med
• 出版时间：11 May, 2012
• 卷：149
• 期：4
• 页码：886-898
• 文件大小：1968 K

摘要

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Summary

The Arc/Arg3.1 gene product is rapidly upregulated by strong synaptic activity and critically contributes to weakening synapses by promoting AMPA-R endocytosis. However, how activity-induced Arc is redistributed and determines the synapses to be weakened remains unclear. Here, we show targeting of Arc to inactive synapses via a high-affinity interaction with CaMKII尾 that is not bound to calmodulin. Synaptic Arc accumulates in inactive synapses that previously experienced strong activation and correlates with removal of surface GluA1 from individual synapses. A lack of CaMKII尾 either in聽vitro or in聽vivo resulted in loss of Arc upregulation in the silenced synapses. The discovery of Arc's role in 鈥渋nverse鈥?synaptic tagging that is specific for weaker synapses and prevents undesired enhancement of weak synapses in potentiated neurons reconciles essential roles of Arc both for the late phase of long-term plasticity and for reduction of surface AMPA-Rs in stimulated neurons.