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. 2018 Oct 2;8:14675. doi: 10.1038/s41598-018-32821-4

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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A proposed model depicts the control of AMPAR surface expression through Arc/PICK1 interaction. Our proposed model suggests a potential mechanism through which Arc is selectively targeted to AMPARs during LTD. Phase I: (1) Ca2+ enters through activated NMDA receptors (2) and binds to PICK1 (3) leading to an electrochemical conformational change allowing PICK1 to preferentially bind to AMPARs. Phase II: (4) A depolarizing event increases the local expression and concentration of Arc protein in the post-synaptic terminal (5) which leads to increased binding to activated PICK1. Phase III: (6) Arc recruits endophilin and (7) dynamin causing membrane curvature (8) and the endocytosis of AMPARs from the plasma membrane.