Figure 5. Effects of different competitive antagonists for glutamate receptors on PPF at GC–IN synapses.

A and B, top, effects of CNQX (0.5 μm, A) and γ-DGG (200 μm, B) on GC–IN synaptic transmission. GC axons were repetitively stimulated with an ISI of 30 ms. Traces represent superimpositions of five successive EPSCs recorded from the IN before (left) and during (middle) drug treatment. After averaging, the depressed first EPSC (black traces) was scaled to the control EPSC (grey traces) and superimposed (right). Bottom, averaged traces of the first (grey traces) and second (black traces) EPSCs were scaled to the same peak amplitude. C and D, the PPR_amp (C) and PPR_decay (D) before (control, open columns) and during treatment with CNQX (0.5 μm, black columns) or γ-DGG (200 μm, grey columns). Each column represents the mean ± SEM (n= 6–7). ***P < 0.001, *P < 0.05. The inhibitory effects of 0.5 μm CNQX and 200 μmγ-DGG on the peak amplitude of the first EPSC were not different significantly (P= 0.69). E and F, time course of changes in the amplitude (E) and decay-time constant (F) of the first (open circles) and second (filled circles) EPSCs during application of γ-DGG (200 μm). EPSCs were evoked every 15 s by test stimulation. The amplitude is expressed as a percentage of the first EPSC, which was determined prior to application of γ-DGG. γ-DGG was applied for 10 min by perfusion (as indicated by the horizontal bar). Each point represents the mean ± SEM (n= 8–11). G–I, summary of the effects of CNQX (black columns) and γ-DGG (grey columns) on the kinetics of the second EPSC, as fitted by a double-exponential procedure. Each column represents the mean ± SEM (n= 6–12).