Fig. 6: Effect of mutations in GluN2D on l-glutamate and UBP791 sensitivity.
From: Structural basis of subtype-selective competitive antagonism for GluN2C/2D-containing NMDA receptors
a Representative TEVC dose-response traces of single mutant GluN1-4a/GluN2D Met763Lys (left panel), Lys766Arg (middle panel) or double mutant Met763Lys/Lys766Arg (right panel) NMDARs held at −60 mV. Currents were evoked by application of 100 μM glycine and 1 μM l-glutamate and inhibited by varying concentrations of UBP791 (Met763Lys: concentration increments: 0.12/0.37/1.1/3.3/10/30/60 μM; for Lys766Arg and double mutant: three-fold increments from 0.08–60 μM). b Averaged dose-response curves (mean ± s.d.) for inhibition with UBP791 from eight, twelve, and six recordings for GluN1-4a/GluN2D Met763Lys, GluN1-4a/GluN2D Lys766Arg, and GluN1-4a/GluN2D Met763Lys/Lys766Arg, respectively, fit with the Hill equation to calculate IC50 and Hill coefficient (nH). c EC50 for l-glutamate and d Ki for UBP791 for the mutants were obtained by TEVC recordings as in Fig. 2. Single data points are shown as open circles, the bar graph represents the mean with error bars for s.d., the number of recordings (n) and the fold-difference to EC50 and Ki of GluN2D (WT) are as shown. Pairwise comparison shows WT and mutants have different potencies (p < 0.05 with two-tail t-test and Bonferroni correction) except where stated (n.s.).
