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. 2017 May 19;28(6):2175–2191. doi: 10.1093/cercor/bhx123

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Figure 2. — The inhibitory effect of D2R activation of PFC pyramidal neuron excitability is reduced whereas the excitatory effect of D1R activation of PFC pyramidal neuron excitability is enhanced in Df(16)A^+/− mice. (A) Bath application of 1 μM quinpirole-induced greater decrease in the cell excitability in WT (N = 7, n = 8, P = 0.014, Wilcoxon test) than Df(16)A^+/− (N = 7, n = 10, Wilcoxon test, P = 0.10) mice. Right panel illustrates the effect of quinpirole on the action potential firing induced by depolarizing current injection (150–250 pA) in single neurons from WT and Df(16)A^+/− mice. (B) Quinpirole decreased cell excitability in a dose-dependent manner (0, 0.4, 0.8, 1.0, and 2.0 μM) in WT mice (before and after quinpirole, 0 μM: N = 3, n = 4, P = 0.50; 0.4 μM: N = 3, n = 4, P = 0.25; 0.8 μM: N = 7, n = 14, P = 0.004; 1 μM: N = 7, n = 8, P = 0.014; 2 μM: N = 5, n = 5, P = 0.04, Wilcoxon test) but led to significantly less decrease in Df(16)A^+/− mice (before and after quinpirole, 0 μM: N = 3, n = 4, P = 0.41; 0.4 μM: N = 3, n = 4, P = 1.00; 0.8 μM: N = 7, n = 11, P = 0.17; 1 μM: N = 7, n = 10, P = 0.10; 2 μM: N = 3, n = 6, P = 0.84, Wilcoxon test; WT vs. Df(16)A^+/−: P = 0.017, two-way ANOVA). (C) Dose-dependent increase in first spike latency in WT mice (before and after quinpirole, 0 μM: n = 4, P = 0.63; 0.4 μM: n = 4, P = 0.25; 0.8 μM: n = 14, P = 0.0004; 1 μM: n = 8, P = 0.02; 2 μM: n = 5, P = 0.03, Wilcoxon test) was greater than Df(16)A^+/− mice (before and after quinpirole, 0 μM: n = 4, P = 0.50; 0.4 μM: n = 4, P = 0.63; 0.8 μM: n = 11, P = 0.30; 1 μM: n = 10, P = 0.16; 2 μM: n = 6, P = 0.31; WT vs. Df(16)A^+/−: P = 0.02, two-way ANOVA). (D) Bath application of 4 μM SKF38393 induced less increase in cell excitability in WT (N = 8, n = 9, P = 0.04, Wilcoxon test) than in Df(16)A^+/− mice (N = 8, n = 12, P = 0.0023, Wilcoxon test) mice. Right panel illustrates the effect of SKF38393 on the action potential firing induced by depolarizing current injection (100–150 pA) in single neurons from WT and Df(16)A^+/− mice. (E) SKF38393 increased cell excitability in a dose-dependent manner (0, 2, 4, and 8 μM) in WT mice (before and after SKF38393, 0 μM: N = 3, n = 4, P = 0.59; 2 μM: N = 4, n = 5, P = 0.13; 4 μM: N = 8, n = 9, P = 0.04; 8 μM: N = 3, n = 5, P = 0.03, Wilcoxon test) but showed significantly greater increase in Df(16)A^+/− mice (0 μM: N = 3, n = 4, P = 0.57; 2 μM: N = 3, n = 5, P = 0.06; 4 μM: N = 8, n = 12, P = 0.0023; 8 μM: N = 3, n = 5, P = 0.02, Wilcoxon test; WT versus Df(16)A^+/−: P = 0.008, two-way ANOVA). (F) Dose-dependent decrease in first spike latency in Df(16)A^+/− mice (before and after SKF38393, 0 μM: n = 4, P = 0.75; 2 μM: n = 5, P = 0.13; 4 μM: N = 8, n = 12, P = 0.0005; 8 μM: n = 5, P = 0.023, Wilcoxon test) was greater than in WT mice (0 μM: n = 4, P = 0.13; 2 μM: n = 5, P = 0.13; 4 μM: n = 9, P = 0.03; 8 μM: n = 5, P = 0.03, Wilcoxon test; WT versus Df(16)A^+/−: P = 0.005, two-way ANOVA). Data are shown as mean ± SEM. *P < 0.05, ^#P < 0.05, **P < 0.01, ^##P < 0.01, ***P < 0.001, ^###P < 0.001.