Figure 4

Treatment with JuA differentially affects sleep loss-induced alterations in WT and APP/PS1 mice. (A) Sample traces showing mEPSCs recorded in the CA1 of the hippocampus in WT + SD, WT + JuA + SD, APP/PS1 + SD and APP/PS1 + JuA + SD groups. (B,C) Quantification of mEPSCs reveals that JuA prevents sleep loss-induced increase in mEPSCs frequency and amplitude between APP/PS1 + SD (n = 10 cells/ 3 mice) and APP/PS1 + JuA + SD (n = 10 cells/ 3 mice) groups; while JuA treatment does not prevent sleep loss-induced decrease in mEPSCs frequency and amplitude in WT + SD (n = 14 cells/ 3 mice) and WT + JuA + SD (n = 15 cells/ 3 mice) group. (D) Sample traces showing mEPSCs recorded in the CA1 of the hippocampus in young WT, WT + JuA, APP/PS1 and APP/PS1 + JuA groups. (E,F) Quantification of mEPSCs amplitude and frequency shows no effect of JuA treatment in non-SD mice (n = 11 cells/ 3 mice for WT, n = 12 cells/ 3 mice for WT + JuA, n = 12 cells/ 3 mice for APP/PS1, n = 12 cells/ 3 mice for APP/PS1 + JuA). (G) Representative immunoblots of hippocampus extracts from APP/PS1, APP/PS1 + SD and APP/PS1 + JuA + SD mice. (H) Quantification of the immunoblots reveals that JuA treatment prevents sleep loss-induced increase in levels of NMDAR and GluR1 and pCaMKII- β and α in APP/PS1 mice. (I) Representative immunoblots of NMDAR, GluR1, pCREB and tCREB from APP/PS1 and APP/PS1 + JuA groups. (J) Quantification reveals no effect of JuA treatment on non-SD mice. Each value represents the mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001; two-sample t-test, one-way ANOVA and two-way ANOVA analysis followed by Tukey’s and LSD post hoc test.