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Arc/Arg3.1 interacts with the endocytic machinery to regulate AMPA receptor trafficking.

Authors: Chowdhury, S  Shepherd, JD  Okuno, H  Lyford, G  Petralia, RS  Plath, N  Kuhl, D  Huganir, RL  Worley, PF 
Citation: Chowdhury S, etal., Neuron. 2006 Nov 9;52(3):445-59.
Pubmed: (View Article at PubMed) PMID:17088211
DOI: Full-text: DOI:10.1016/j.neuron.2006.08.033

Arc/Arg3.1 is an immediate-early gene whose mRNA is rapidly transcribed and targeted to dendrites of neurons as they engage in information processing and storage. Moreover, Arc/Arg3.1 is known to be required for durable forms of synaptic plasticity and learning. Despite these intriguing links to plasticity, Arc/Arg3.1's molecular function remains enigmatic. Here, we demonstrate that Arc/Arg3.1 protein interacts with dynamin and specific isoforms of endophilin to enhance receptor endocytosis. Arc/Arg3.1 selectively modulates trafficking of AMPA-type glutamate receptors (AMPARs) in neurons by accelerating endocytosis and reducing surface expression. The Arc/Arg3.1-endocytosis pathway appears to regulate basal AMPAR levels since Arc/Arg3.1 KO neurons exhibit markedly reduced endocytosis and increased steady-state surface levels. These findings reveal a novel molecular pathway that is regulated by Arc/Arg3.1 and likely contributes to late-phase synaptic plasticity and memory consolidation.

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CRRD Object Information
CRRD ID: 10047209
Created: 2015-07-11
Species: All species
Last Modified: 2015-07-11
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.