Figure 2.

Anti-NKCC1 amiR treatment rescues inhibitory GABAergic signaling in Ts65Dn neurons in culture

(A) Left: schematic representation of the LV expressing either control or NKCC1 amiRs. Right: symbol legend for panels (B)–(E). (B) Quantification of the average spontaneous spiking activity recorded in cell-attached, patch-clamp configuration in LV-transduced hippocampal neurons (16–20 DIVs) from WT and Ts65Dn mice before and after bath application of the GABA_AR antagonist bicuculline (10 μM). (C) Example traces and spiking frequency of single, active cells, from experiments in (B) for LV-transduced WT and Ts65Dn neurons before (baseline) and during bath application of bicuculline. (D) Quantification of the average spontaneous spiking activity recorded in cell-attached patch-clamp configuration in LV-transduced hippocampal neurons (16–20 DIVs) from WT and Ts65Dn mice before and after bath applications of increasing concentrations of GABA (1–200 μM). (E) Example traces and spiking frequency of single, active cells, from experiments in (D) for LV-transduced WT and Ts65Dn neurons before (baseline) and during bath application of GABA at 100 μM. Data shown in (B) and (D) are means ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, Tukey post hoc test after two-way RMs-ANOVA. In (C) and (E), the numbers in parentheses indicate the number of active cells recorded before and after drug application for each experimental group, and boxed numbers indicate the percentages of cells showing at least a 20% increase (↑) or decrease (↓) in spiking frequency. ^#p < 0.05, ^##p < 0.01, ^###p < 0.001, paired Student’s t test or Wilcoxon signed-rank test.