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. 2020 Jun 9;10:186. doi: 10.1038/s41398-020-00878-3

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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. 2 — a Western blot analysis of postsynaptic density-95 (PSD-95) and β-actin in the prefrontal cortex (PFC) of the four groups (two-way ANOVA: LPS: F_1,36 = 15.53, P = 0.0004; SDV: F_1,36 = 1.028, P = 0.3174; interaction: F_1,36 = 9.131, P = 0.0049). b Western blot analysis of AMPA receptor subunit GluR1 (GluA1) and β-actin in the PFC of the four groups (LPS: F_1,36 = 8.377, P = 0.0064; SDV: F_1,36 = 1.229, P = 0.2749; interaction: F_1,36 = 7.055, P = 0.0117). The data represent mean ± S.E.M (n = 10). *P < 0.05, ***P < 0.0001; N.S. not significant. c There was a positive correlation (r = 0.422, P = 0.007) between PSD-95 and GluA1. d There was a negative correlation (r = −0.334, P = 0.035) between FST immobility time and PSD-95 in the PFC. e There was a negative correlation (r = −0.557, P < 0.001) between PSD-95 in the PFC with plasma IL-6. f There was a negative correlation (r = −0.567, P < 0.001) between PSD-95 in the PFC and plasma TNF-α. g There was a negative correlation (r = −0.460, P = 0.003) between GluA1 in the PFC and plasma IL-6. h There was a negative correlation (r = −0.386, P = 0.014) between GluA1 in the PFC and plasma TNF-α.