Figure 5
Changes in AMPAR subunit composition does not alter the properties of NMDARs. (A) Outward Schaffer collateral evoked NMDAR-mediated EPSCs (Vhold = +50 mV, in DNQX) and inward AMPAR-mediated EPSCs (Vhold = −70 mV, in Mg2+) recorded from WT, GluA2 KO, and GluA1-3 KO CGE interneurons in P5-9 and P17–21 mice. As early as P5, all interneurons exhibited both AMPA and NMDAR-mediated evoked activity. NMDAR-mediated EPSCs were evoked at a reasonably fixed amplitude of ~100–150 pA revealing only a small corresponding AMPAR-mediated component in CGE GluA1-3 KO interneurons. (B) Scatter plots of NMDA:AMPA ratios for all three mouse lines at two different developmental time points. Elimination of GluA1-3 subunits but not the GluA2 subunit increases the NMDA:AMPA EPSC ratio largely through a reduction in the corresponding AMPAR-mediated EPSC. (C) NMDAR-mediated EPSCs (Vhold = +50 mV) in the presence (smaller traces) and absence (larger traces) of the GluN2B-expressing NMDAR blocker ifenprodil, recorded from WT, GluA2 KO and GluA1-3 KO CGE interneurons from P5-9 and P17-21 mice. (D) Scatter plots of the NMDAR-mediated decay tau of NMDAR-mediated EPSCs and the magnitude of ifenprodil block of the NMDAR-mediated EPSC. The data for all three groups were compared for significance with ANOVA and a posthoc Wilcoxon-Mann-Whitney Test when a significance was found with ANOVA. *p < 0.05; ***p < 0.0005.
