Figure 5

Abnormal neuronal oscillations and sensitivity to NMDAR channel blocker due to loss of GluN2C subunit.
(A) Representative ECoG recordings of WT, GluN2C HET, and GluN2C KO mice display typical awake responses. (B) Representative power spectrum analyses of responses before and after MK-801 administration in WT, GluN2C HET, and GluN2C KO mice as indicated. (C) Average percent increase in the power spectrum in WT (n = 6), GluN2C HET (n = 4), and GluN2C KO mice (n = 4) in response to MK-801 administration (0.2 mg/kg IP). Shaded areas represent S.E.M. (D) Effect of phencyclidine on spontaneous alternation in Y-maze (n = 11–13 for WT, 11 for GluN2C HET and 12–13 for GluN2C KO). PCP (1 mg/kg) reduced the percent alternation in GluN2C HET and KO mice (Bonferroni’s multiple comparison, *P < 0.05, **P < 0.01) but not in GluN2C WT mice. At 3 mg/kg PCP induced impairment in spontaneous alternation in all genotypes (***P < 0.001).