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. 2016 Dec 14;36(50):12640–12649. doi: 10.1523/JNEUROSCI.2980-16.2016

Figure 3.

Figure 3.

NMDAR adaptation to Tat requires activation of GluN2A-containing NMDARs, but not GluN2B-containing NMDARs. A, Representative traces showing NMDA-evoked steady-state whole-cell current from cells treated with Tat for 24 h in the absence and presence of NVP-AAM007 (50 nm) for 15 min before and during treatment with Tat. NMDA (10 μm) was applied at the time indicated by the horizontal bar. Scale bar, 100 pA, 60 s. B, Bar graph summarizing the NMDA-evoked steady-state whole-cell current amplitudes normalized to whole-cell capacitance from untreated (open bars) neurons or neurons treated with Tat (solid bars) for 24 h in the presence or absence of NVP-AAM007. C, Representative traces showing NMDA-evoked (10 μm NMDA) steady-state whole-cell current from cells treated with Tat for 24 h in the absence and presence of ifenprodil (3 μm) for 15 min before and during treatment with Tat for 24 h. Scale bar, 100 pA, 60 s. D, Bar graph summarizing the NMDA-evoked steady-state whole-cell current amplitudes normalized to whole-cell capacitance from neurons untreated (open bars) or treated with Tat (solid bars) for 24 h in the presence or absence of ifenprodil (n ≥ 6 for all groups) Data are shown as mean ± SEM. *p < 0.05 relative to all other groups (one-way ANOVA with Tukey's post hoc test).