Figure 6.

DHA potentiation requires the GluN2 CTD. A, Exposure to 15 μm DHA (shaded bars) did not potentiate whole-cell currents evoked by 10 μm NMDA plus 10 μm glycine (open bars) in HEK cells cotransfected with truncated GluN1₈₄₀ and GluN2B₈₄₆ (top trace), or for cotransfection of a wild-type and a truncated subunit: GluN1₈₄₀/GluN2B_wt (middle trace), GluN1_wt/GluN2B₈₄₆ (bottom trace). B, Exposure to 15 μm DHA (shaded bar) potentiated whole-cell current evoked by 10 μm NMDA plus 10 μm glycine (open bars) in an HEK cell transfected with a GluN1 chimera bearing a GluK2 CTD and wild-type GluN2B (top); lack of effect of DHA on wild-type GluN1 with the GluN2B chimera bearing a GluK2 CTD (bottom). C, Plot of current (mean ± SEM) evoked immediately after exposure to DHA as a fraction of control current before DHA treatment for wild-type and truncated or chimeric NMDA receptor subunits. *, Significant difference from wild-type (p < 0.0001, ANOVA on ranks with post hoc Dunn's test) and not significantly different from no effect (i.e., I_DHA/I_control = 1, t-statistic). # denotes that for the N1 (K2CTD)/N2 wild-type combinations I_DHA/I_control was significantly >1 but also significantly less than that for wild-type receptors. Inset, Proximal CTD sequences of GluN1, GluN2A, and GluN2B. Shading denotes truncation after N1 H840, 2A L845, and 2B F846.