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
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).
