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. 2018 Jul 11;38(28):6388–6398. doi: 10.1523/JNEUROSCI.0447-18.2018

Figure 5.

Figure 5.

α2δ-1 Ablation abolishes the potentiating effect of Ang II on presynaptic and postsynaptic NMDAR activity in spinally projecting PVN neurons of mice. A, B, Original traces (A) and mean changes (B) show NMDAR currents elicited by puff application of 100 μmol/L NMDA to labeled PVN neurons in brain slices treated with vehicle or 2 μmol/L Ang II in wild-type (WT, vehicle: n = 11 neurons; Ang II: n = 9 neurons) and Cacna2d1 knock-out (KO, vehicle: n = 14 neurons; Ang II: n = 10 neurons) mice. ***p < 0.001 compared with the WT vehicle group. ###p < 0.001 compared with the WT Ang II group. C–F, Representative traces and cumulative plots of mEPSCs in labeled PVN neurons of WT and Cacna2d1 KO mice before bath application of 50 μmol/L AP5 (Baseline), with bath application of 50 μmol/L AP5 (AP5), and after washout (Washout) in brain slices treated with vehicle or 2 μmol/L Ang II. G, H, Mean changes show the effect of AP5 on the frequency and amplitude of mEPSCs in the labeled PVN neurons of brain slices from WT mice (n = 8 neurons per group) and Cacna2d1 KO mice (n = 9 neurons per group) treated with vehicle or with 2 μmol/L Ang II. Data are presented as means ± SEM. ***p < 0.001 compared with the baseline value of WT mice treated with vehicle. ##p < 0.01, ###p < 0.001 compared with the baseline value of WT mice treated with Ang II.

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