Altered NMDA EPSCs and synaptic plasticity in the dentate GCs. (A) Altered current–voltage relationship of NMDA EPSCs in mutant GCs. The amplitudes of NMDA EPSCs at each potential were normalized to that at +40 mV and plotted against the holding potential. Relative EPSC amplitudes at −60 mV and −80 mV were significantly different between control (open circles, n = 13) and mutant (filled circles, n = 15) mice (p < 0.005). (B) Sample recordings of NMDA EPSCs at +40, −20, and −80 mV. Stimulus artifacts are truncated. (C) Relative amplitudes of NMDA EPSCs at −80 mV. Each symbol represents a single cell. (D) Input–output relationship of fEPSPs recorded from the DG (n = 15 each). (E) Enhanced short-term potentiation in mutant mice. Tetanic stimulation (100 Hz for 0.5 s repeated 4 times) was applied at time 0. The magnitude of potentiation just after tetanic stimulation was significantly larger in the mutants (p < 0.001, n = 8 each). (F) Facilitated induction of LTP in mutant mice. The same pattern of tetanic stimulation as in (E) was applied at twice the test intensity. The magnitude of potentiation 25–30 min after the tetanic stimulation was significantly greater in the mutants (p < 0.01, n = 7 each). Sample recordings on the right were obtained at the times indicated by the numbers. All values are expressed as the mean ± S.E.M. Statistical significance was evaluated using two-tailed Mann–Whitney tests, Student’s t-tests, or ANOVA.