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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Neuropharmacology. 2016 Nov 19;114:20–33. doi: 10.1016/j.neuropharm.2016.11.013

Fig. 3. Comparison of glutamate potency and desensitization among GluN2A F636/F637 dual mutant subunits.

Fig. 3

A–B, Bar graphs show the average EC50 values for glutamate-activated peak (Ip, A) and steady-state (Iss, B) currents in lifted HEK 293 cells expressing GluN1 and wild- type GluN2A subunits (F/F, gray) or various GluN1/GluN2A(F636/F637) mutant subunits. Asterisks indicate EC50 values that differed from the wild-type value (***P < 0.001; one-way ANOVA). Results are the means ± S. E of 5–12 cells. C, Graph plots values of glutamate log EC50 for peak current in the series of mutants versus values of glutamate log EC50 for steady- state current; these values were significantly correlated (R2 = 0.93, P < 0.001). The line shown is the least-squares fit to the data. D, Bar graph shows the average values of maximal steady-state to peak current ratio (Iss:Ip) in lifted cells coexpressing GluN1 and wild-type GluN2A subunits (F/F, gray) or various GluN1/GluN2A(F636/F637) mutant subunits. Currents were activated by 300 μM glutamate in the presence of 50 μM glycine. Asterisks indicate values that differed significantly from the wild-type value (*P < 0.05, **P < 0.01; one-way ANOVA). Results are the means ± S. E of 5–12 cells.