CRF increases NMDA receptor-mediated transmission through CRF1 and PKA. (A-D) CRF (10 nM) increased a small pharmacologically (bicuculline, 30 μM; NBQX, 20 μM) isolated NMDA component recorded at a holding potential of +20 mV that was blocked by an NMDA receptor antagonist (AP5, 50 μM; not shown). Bar histograms show averaged data (mean ± SE). Individual traces are the average of 8–10 EPSCs recorded at +20 mV. (A) A CRF1 receptor antagonist (NBI27914, 1 μM, n = 5) inhibited the facilitatory effect of CRF. (B) A CRF2 receptor antagonist (astressin-2B, AStr2B, 1 μM, n = 5) had no effect. (C) A PKA inhibitor (KT5720, 1 μM, n = 5) blocked the CRF-induced facilitation. (D) A PKC inhibitor (GF109203x, 1 μM, n = 5) had no effect. Drugs were applied for 12–15 min. ** P < 0.01; ns (not significant) P > 0.05; ANOVA with Bonferroni posttests. Statistical analysis was performed on raw data.