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. 2022 Aug 10;23(1):98. doi: 10.1186/s10194-022-01469-x

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — DRD2 agonist treatment attenuates central sensitization via the PI3K signaling pathway. A, B and C The PI3K activator 740YP reversed the anti-injury effects of the DRD2 agonist quinpirole and reduced pain thresholds in CM rats. Two-way ANOVA with the Bonferroni post hoc test; n = 6/group; **P < 0.01, ***P < 0.001 vs. the Sham + DMSO group; ###P < 0.001 vs. the CM + DMSO group. D and E 740YP reversed the DRD2-mediated reductions in the protein expression of PSD95 and phosphorylation of ERK. F and G 740YP abolished the effects of the DRD2 agonist on reducing GLUA1 membrane trafficking and p-GLUA1 levels. One-way ANOVA with Dunnett’s post hoc test; n = 6/group; **P < 0.01, ***P < 0.001 vs. the Sham + DMSO group; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. the CM + DMSO group