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. 2020 Nov 24;11:5962. doi: 10.1038/s41467-020-19780-z

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© The Author(s) 2020

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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Fig. 8 — a Simplified scheme of PRDM5-MAGL-2-AG-CB1R pathway in normal mice. b Simplified scheme of PRDM5-MAGL-2-AG-CB1R pathway in mice under ketamine conditioning paradigm. Ketamine represses Mgll gene transcription by enhancing the binding of PRDM5 at the promoter of gene Mgll, leading to the decreased MGL expression and 2-AG hydrolysis. Consequently, increased 2-AG activates CB1R signaling, resulting in ketamine addiction-related dendritic remodeling and behaviors.