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. 2019 Feb 19;116(14):7113–7122. doi: 10.1073/pnas.1820690116

Fig. 5.

Fig. 5.

Overactive mTOR signaling enhances AMPAR expression in EE-experienced CA1-RARα KO mice. (A) Immunoblot analysis of mTOR and phospho-mTOR in home cage (HC)- and EE-exposed WT and CaMKII-Cre RARα KO CA1 [one-way ANOVA with Tukey’s multiple comparison test: F(4,17) = 6.857, P = 0.0018, **P < 0.01]. (B) Immunoblot analysis of ribosomal protein S6 and phospho-S6 in CA1 [one-way ANOVA with Tukey’s multiple comparison test: F(4,22) = 8.143, P = 0.0003, **P < 0.01]. (C) Rapamycin treatment during EE experience restores AMPAR levels back to normal in the CA1 of RARα cKO mice. Immunoblot analysis of total GluA1 and GluA2 expression in HC- and EE-experienced RARα KO CA1 with and without rapamycin [one-way ANOVA with Tukey’s multiple comparison test: GluA1: F(2,18) = 8.433, P = 0.0026; GluA2: F(2,18) = 4.558, P = 0.025, *P < 0.05, **P < 0.01]. (D) Immunoblot analysis of MAP kinase ERK and phospho-ERK in CA1 [two-way ANOVA test: HC/EE × WT/KO: F(1,15) = 36.51, P < 0.0001; Tukey post hoc test: ****P < 0.0001]. (E) Immunoblot analysis of AKT and phospho-AKT in CA1 [two-way ANOVA test: HC/EE × WT/KO: F(1,13) = 0.2659, P > 0.5]. All graphs represent mean ± SEM.