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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Brain Behav Immun. 2020 Aug 26;90:226–234. doi: 10.1016/j.bbi.2020.08.022

Fig. 3.

Fig. 3.

Administration of (+)-naloxone reduces the levels of IFNβ and TNFα induced by stress. (A-F) Wild-type non-shocked (Control) mice or mice subjected to inescapable foot shocks (IES) were administered the TLR4 antagonist (+)-naloxone (5 mg/kg; i.v.) or vehicle 1 h prior to IES and sacrificed 12 h after IES. (A) Hippocampal levels of IFNβ. Each point represents an individual mouse. Bars represent means ± SEM. One-way ANOVA, F(2,17) = 4.969, Dunnett post-hoc test, *p < 0.05, compared to control mice, n = 4–8 mice/group. (B) Plasma and (C) hippocampal levels of TNFα. Each point represents an individual mouse. Bars represent means ± SEM. One-way ANOVA, (B) F(2,14) = 3.479, (C) F(2,14) = 5.930, Dunnett post-hoc test, *p < 0.05, compared to control mice, n = 3–8 mice/group. Hippocampal levels of (D) IL-17A, (E) IL-1β and (F) IL-6. Each point represents an individual mouse. Bars represent means ± SEM. One-way ANOVA, (D) F (2,17) = 8.942, (E) F(2,16) = 6.960, (F) F(2,17) = 4.057, Dunnett post-hoc test, *p < 0.05, **p < 0.01, compared to control mice, n = 4–8 mice/group.