Extended Data Fig. 7: GluN2B was not responsible to the effects of MK-801 in intrinsic excitability and antidepressant-like behaviors, related to Fig. 6.
From: GluN2A mediates ketamine-induced rapid antidepressant-like responses
a, Representative recording traces after injection of 330 pA depolarizing current in CA1 pyramidal neurons treated with Veh or 3 μM Ro-25 6981 for 1–2 hours. b and c, Quantitation of the number of action potentials (b) after injection of depolarizing currents and RMP (c) recorded from neurons after Veh or Ro-25 6981 treatments (Veh n = 18, Ro 25-6981 n = 19). d–i, number of AP (e, p = 0.0074), RMP (f, p = 0.041), current-voltage curve (h, p = 0.00070), input resistance (RIn) (i, p = 0.00080) and sample trace recorded from CA1 pyramidal neurons after incubated with ‘Ro 25-6981 + Veh’ (n = 10) or ‘Ro 25-6981 + 10 μM MK-801’ (n = 10) for 1–2 hours from WT mice (g). j and k, Effects of MK-801 on WT mice-treated with GluN2B inhibitor Ro 25-6981 (10 mpk) were evaluated with TST (j; Ro 25-6981 + Sal n = 10; Ro 25-6981 + MK-801 n = 10, p < 0.0001) and FST (k; Ro 25-6981 + Sal n = 10; Ro 25-6981 + MK-801 n = 9, p < 0.0001). All the recordings were measured from CA1 pyramidal neurons acutely prepared from 6-8 weeks old WT mice. Error bars show SEM. Two-way ANOVA (b, e, h) or Student’s t test (two-tailed) (c, f, i, j, k). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.