FIGURE 4.

D1 receptor modulation modifies NR2A/NR2B ratio in corticostriatal slices. A, Western blot (WB) analysis of NR2A and NR2B subunits from the striatal homogenate and TIF fraction obtained from control (C) and SKF38393-treated (10 μm, 45 min) corticostriatal slices. The same amount of protein was loaded in each lane. The bar graph shows the amount of NR2A and NR2B subunits in the homogenate and TIF fraction from SKF38393-treated slices (t test; ***, p < 0.001). B, total homogenate was immunoprecipitated (i.p.) with antibody against D1 receptor and the presence of D1 and NR2A in the immunocomplex was evaluated by Western blot. Treatment with SKF38393 reduces NR2A co-precipitation with D1 (t test; **p < 0.005). C, Western blot of NR2A and NR2B subunits from control and SKF38393-treated corticostriatal slices exposed (+BS³ lanes) or not (−BS³ lanes) to the cross-linking agent BS³. NMDA receptor subunits high-molecular weight complexes that did not enter the gel are not shown (t test; *, p < 0.05, NR2B, SKF38393 versus control). D, Western blot analysis of NR2A and NR2B subunits from the homogenate and TIF fraction obtained from control and SCH23390-treated (SCH, 45 min) corticostriatal slices. The same amount of proteins was loaded in each lane (t test; *, p < 0.05). E, Western blot of GluR1 and GluR2 subunits from control and SKF38393-treated corticostriatal slices exposed (+BS³ lanes) or not (−BS³ lanes) to the cross-linking agent BS³. AMPA receptor subunits high-molecular weight complexes that did not enter the gel are not shown (t test; *, p < 0.05, GluR1, SKF38393 versus control; t test, **, p < 0.01, GluR2, SKF38393 versus control).