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. 2021 Jan 28;11:2567. doi: 10.1038/s41598-021-82206-3

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© This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Illustration of the activation of MAPK/MSK signaling pathway in LgA-H rats. Intake of large amount of oxycodone during long-access over 20 days caused increased phosphorylation of PKC, ERK1/2, MSK1, and MSK2. Increased MSK phosphorylation is accompanied by increased histone H3 phosphoacetylation and CREB phosphorylation. In addition, there were increases in the protein expression of two acetyltransferases, CBP and Tip60 that acetylate H3K27. Recruitment of CBP by CREB and histone modifications serve to create a permissible transcriptional environment that led to increased mRNA levels of GluA2 and GluA3 in a MSK1-dependent fashion. This kinase-histone modification cascade may serve as targets for therapeutic interventions against oxycodone use disorder.