Figure 7.
GluD2 channel function and ligand binding ability are not required for the recovery of impaired PF–Purkinje cell synapses in GluD2-null mice. A, B, Schematic diagrams of mutant GluD2s and representative PF–EPSCs recorded from GluD2-null Purkinje cells expressing GFP plus GluD2V/R (GluD2V/R, A) or GFP plus GluD2R/K (GluD2R/K, B). The valine at position 617 in the selectivity filter domain (indicated by a star in A) was replaced with arginine and the arginine at position 530 in the putative ligand binding site (indicated by × in B) was replaced with lysine to produce the “pore-dead mutant” and “ligand binding-dead mutant,” respectively. C, Averaged input–output (I-O) relationship of the PF–EPSCs. The PF–EPSC amplitudes from GluD2-null Purkinje cells expressing GFP (Vector), GFP plus GluD2wt (GluD2wt), GFP plus GluD2V/R (GluD2V/R), or GFP plus GluD2R/K (GluD2R/K) were averaged. The error bars indicate the SEM. D, Results for the rotor-rod test. Mice were placed on the rotor-rod at 20 rpm before (Pre) and 1 d after (Post) receiving a subarachnoidal injection of Sin–GFP (Vector), Sin–GluD2wt–GFP (GluD2wt), Sin–GluD2V/R–GFP (GluD2V/R), or Sin–GluD2R/K–GFP (GluD2R/K). The average time was calculated from the results of six trials. For comparison, the data for Sin–GFP and Sin–GluD2wt–GFP in C and D were taken from Figures 5 and 1, respectively. *p < 0.05, **p < 0.01. ns, Not significant.