Fig. 4

D1R antagonists do not block the inhibitory effect of SKF 81297 on eEPSCs. a I: Averaged traces of AMPAR mediated currents and time course for the application of the D1R antagonist SCH-23390 60 μM and the D1R agonist SKF 81297 30 μM. II: Averaged and normalized data for eEPSC amplitudes, before, during and following application of SCH-23390 60 μM and SKF 81297 30 μM (n = 6/5mice). b I: Averaged traces and time course of AMPAR mediated currents for the application of the D1R antagonist SCH-23390 10 μM and the D1R agonist SKF 81297 10 μM. II: Averaged and normalized data for eEPSC amplitudes, before, during and following application of SCH-23390 10 μM and SKF 81297 10 μM (n = 7/4 mice). c I: SKF 81297 30 μM produces a robust inhibition of eEPSCs when administered in the presence of the D1R antagonist, SCH-23390 60 μM, which returned towards baseline following washout (one-way ANOVA, F_2,12 = 63.63, p < 0.0001). II: SKF 81297 10 μM produces a robust inhibition of eEPSCs when administered in the presence of the D1R antagonist, SCH-23390 60 μM, which returned towards baseline following washout (one-way ANOVA, F_2,18 = 3.92, p = 0.03). d Comparison of percent inhibition of eEPSCs by SKF 81297 and SCH-23390 at different doses (independent t-test, t₁₀ = 3.51, p = 0.006). e I: Averaged traces with normalized and average data (n = 5/3 mice). II: The D1R antagonist SCH 39166 10 μM does not block the inhibitory effect that SKF 81297 10 μM has on eEPSC amplitude. Following washout EPSCs remained depressed relative to the baseline (one-way ANOVA, F_2,8 = 25.4, p < 0.0001). f I: Averaged traces with normalized and average data for application of SCH 39166 (n = 5/4 mice). II: Application of SCH 39166 10 μM alone inhibits AMPAR mediated eEPSCs, which returned to baseline following washout (one-way ANOVA, F_1,5 = 29.89, p = 0.002). *p < 0.05, **p < 0.01