Figure 4. LTP improvement by RXR activation is PPARα and sex dependent.

(A) Schematic drawing of the top view of a mouse brain. Stars: ipsi and contralateral injection sites of Ppara and scramble shRNA AAV (AAV-ShPpara [orange] and AAV-ShSc [blue]). (B–D) Dashed line represents the plane of the coronal section used in (B–D) for biochemical analyses. (B) RT-qPCR analyses of Ppara mRNA levels in male (♂) and female (♀) Tg mice hippocampi AAV-ShSc and AAV-ShPpara injected at 9–10 mo. Results are expressed as percentage of AAV-ShSc–injected male mice (n = 4 of each; *P < 0.05, **P < 0.01, ***P < 0.001, ns: not significant (P > 0.05), ANOVA followed by Bonferroni’s multiple-comparison posttest). Right panels: PPARα semi-quantitative RT-PCR. (C, D) Representative Western blots of hippocampal lysates from male (♂, in C) and female (♀, in D) Tg mice AAV-ShSc and AAV-ShPpara injected. Right panels: quantification of GluN2A, GluN2B, and GluA1/α tubulin ratios in male (in C) and female (in D) Tg mice AAV-ShSc and AAV-ShPpara injected. Results are expressed as percentage of corresponding Tg mice AAV-ShSc injected (n = 4 in each condition, **P < 0.01, t test; ns: not significant [P > 0.05]). (E, F) CA1 LTP in hippocampal slices from male (♂, in (E)) and female (♀, in (F)) transgenic (Tg) 5xFAD mice (9–10 mo) AAV-ShPpara and AAV-ShSc injected and perfused with 4 μM bexarotene (bex) (n = 4 in each group, ***P < 0.001, t test). Data information: data are presented as mean ± SEM.

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