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Inverse synaptic tagging of inactive synapses via dynamic interaction of Arc/Arg3.1 with CaMKIIbeta.

Authors: Okuno, H  Akashi, K  Ishii, Y  Yagishita-Kyo, N  Suzuki, K  Nonaka, M  Kawashima, T  Fujii, H  Takemoto-Kimura, S  Abe, M  Natsume, R  Chowdhury, S  Sakimura, K  Worley, PF  Bito, H 
Citation: Okuno H, etal., Cell. 2012 May 11;149(4):886-98. doi: 10.1016/j.cell.2012.02.062.
Pubmed: (View Article at PubMed) PMID:22579289
DOI: Full-text: DOI:10.1016/j.cell.2012.02.062

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 CaMKIIbeta 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 CaMKIIbeta either in vitro or in vivo resulted in loss of Arc upregulation in the silenced synapses. The discovery of Arc's role in "inverse" 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.

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RGD Object Information
RGD ID: 8553506
Created: 2014-05-08
Species: All species
Last Modified: 2014-05-08
Status: ACTIVE



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