Figure 8.
Proximal GluN2 CTD substitutions prevent DHA potentiation. A, Plot of current (mean ± SEM) evoked immediately after exposure to DHA as a fraction of control current before DHA treatment for NMDA receptors with wild-type GluN1 and the indicated substitutions to full-length GluN2. Residues highlighted in yellow are wild-type. *, Significant difference from wild-type (p < 0.0001, ANOVA on ranks with post hoc Dunn's test) and not significant difference from no effect (IDHA/Icontrol = 1, t-statistic). # denotes that for the N1 wt/N2A Y842F combination IDHA/Icontrol was significantly >1 but also significantly less than for wild-type receptors. B, Traces show the quadruple FAAA mutant lacked potentiation by DHA (top trace). Potentiation was preserved for the Y842F substitution, in some cases reaching the level observed for wild-type receptors (bottom trace).