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. 2021 Dec 2;16(12):3005–3019. doi: 10.1016/j.stemcr.2021.11.003

Figure 1.

Figure 1

Genetic ablation of aNSCs improved LTP in the hippocampal CA1 of APP/PS1 mice

(A) Timeline for the experiments.

(B and G) Representative traces showing LTP in CA1 of 6-month-old (B) and 4-month-old (G) NTG-TK and NTG-TK+ mice treated with GCV.

(C and H) Representative traces showing LTP in CA1 of 6-month-old (C) and 4-month-old (H) APP/PS1-TK and APP/PS1-TK+ mice treated with GCV.

(D and I) Representative traces showing LTP in CA1 of 6-month-old (D) replotted from (B and C) and 4-month-old (I) replotted from (G and H) NTG-TK, NTG-TK+, APP/PS1-TK, and APP/PS1-TK+ mice treated with GCV.

(E) Quantification of the last 15 min of fEPSP recordings in 6-month-old mice (NTG-TK, n = 6 slices from 3 mice; NTG-TK+, n = 6 slices from 5 mice; APP/PS1-TK, n = 6 slices from 5 mice; APP/PS1-TK+, n = 9 slices from 7 mice). Two-way ANOVA: genotype (APP), F(1,23) < 0.0001, p = 0.9965; ablating aNSCs, F(1,23) = 6.949, p = 0.0148; interaction, F(1,23) = 7.599, p = 0.0112; ∗∗p < 0.01 with Bonferroni post hoc test. Data are represented as mean ± SEM.

(J) Quantification of the last 15 min of fEPSP recordings in 4-month-old mice treated with GCV (NTG-TK, n = 8 slices from 4 mice; NTG-TK+, n = 10 slices from 3 mice; APP/PS1-TK, n = 8 slices from 3 mice; APP/PS1-TK+, n = 10 slices from 3 mice). Two-way ANOVA: genotype (APP), F(1,32) = 4.975, p = 0.0329; ablating aNSCs, F(1,32) = 1.252, p = 0.2715; interaction, F(1,32) = 35.81, p < 0.0001; ∗∗p < 0.01, ∗∗∗p < 0.001 with Bonferroni post hoc test. Data are represented as mean ± SEM.

(F and K) The strength of basal synaptic transmission reflected by input/output (I/O) relationships at the Schaffer collateral-CA1 synapses of 6-month-old (F) and 4-month-old (K) NTG-TK, NTG-TK+, APP/PS1-TK, and APP/PS1-TK+ mice treated with GCV. Two-way ANOVA, data are represented as mean ± SEM. See also Figures S1–S4.