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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. 5. Dual mutations at GluN2A(F636/F637) can alter NMDA receptor ethanol sensitivity.

Fig. 5

A, Traces are currents activated by 10 μM glutamate and 50 μM glycine and their inhibition by 100 mM ethanol (EtOH) in cells expressing GluN1 and GluN2A wild-type (F/F) or 636/637 mutant subunits. B, Concentration-response curves for ethanol inhibition of glutamate-activated current in cells expressing various substitution mutations at GluN2A(F636/F637). Data are the means ± S.E. of 5–12 cells; error bars not visible were smaller than the size of the symbols. Curves shown are the best fits to the equation given in the Materials and Methods. The black curve shows the fit for the wild-type GluN2A subunit. C, Bar graph shows the average IC50 values for ethanol inhibition of glutamate-activated current in cells expressing GluN1 and wild-type GluN2A subunits (F/F) or GluN2A subunits containing various mutations at F636 and F637. Asterisks indicate IC50 values that are significantly different from the wild- type value (*P < 0.05; **P < 0.01; one-way ANOVA). Results are the means ± S. E of 5–12 cells. The wild-type value is from Ren et al. (2012).