Figure 6. Postsynaptic NMDA receptor activation facilitates GABAergic transmission.
A, voltage protocol for NMDAR activation by endogenous glutamate. Experiments were performed upon preloading with tryptophan, and recorded in the presence of CNQX (1 μm), L-CGG-III (10 μm) and CPPG (30 nm) in addition fluoxetine (10 μm). B and C, example traces of IPSCs at start (B, shown by left box in A) and more toward the end (C, right box in A) at −30 mV (calibration 20 pA, 20 ms). D, at −30 mV the specific NMDA antagonist APV (50 μm) significantly suppressed the tonic increase in sIPSC frequency (n = 7, ANOVA followed by a post hoc Bonferroni multiple comparison test, *P < 0.05). E, at −30 mV the 5-HT2 antagonist ketanserin (1 μm) also significantly suppressed the tonic increase sIPSC frequency (n = 7, ANOVA followed by a post hoc Bonferroni multiple comparison test, *P < 0.05).