Extended Data Fig. 6: Cell type specific removal of GluN2A did not alter excitatory or inhibitory synaptic transmission of CA1 pyramidal neurons, related to Fig. 6.
From: GluN2A mediates ketamine-induced rapid antidepressant-like responses
![Extended Data Fig. 6](http://media.springernature.com/full/springer-static/esm/art%3A10.1038%2Fs41593-023-01436-y/MediaObjects/41593_2023_1436_Fig13_ESM.jpg)
a–f, Representative traces (a, d), average individual events (b, e), quantitation of cumulative probability and average amplitude of events (c, f) of mIPSCs and sIPSCs recorded from 4–6 weeks old Nex-2A WT (black) or Nex-2A cKO (olive) mice (mIPSCs: Nex-2A WT n = 12, Nex-2A cKO n = 14; sIPSCs: Nex-2A WT n = 16, Nex-2A cKO n = 14). g–r, Representative traces, average individual events, quantitation of cumulative probability and average amplitude of events of mIPSCs (g–i), sIPSCs (j–l), mEPSCs (m–o) and sEPSCs (p–r) recorded from vGAT-2A WT (black) or vGAT-2A cKO (purple) mice. (mIPSCs: vGAT-2A WT n = 18, vGAT-2A cKO n = 21; sIPSCs: vGAT-2A WT n = 15, vGAT-2A cKO n = 13; mEPSCs: vGAT-2A WT n = 13, vGAT-2A cKO n = 10; sEPSCs: vGAT-2A WT n = 12, vGAT-2A cKO n = 16) 6–8 weeks mcie were used for electrophysiological recordings. Error bars showed SEM. Cumulative frequency was analyzed with Kolmogorov-Smirnov test. Peak amplitudes were analyzed with Student’s t test (two-tailed).