Fig. 2. DA induced the ERK activation via D1 DA receptor and PKA dependent signaling pathway.
Striatal neurons were pretreated for 15 min with vehicle or with the following compounds: SCH 23390 (1 μM), SMBS (20 μM), KT5720 (1 μM) or U0126 (1 μM), and then treated with 10 μM of either DA [A] or SKF R-38393 [B] for 20 min. Immunoblot analysis of p-ERK1/2 expression was conducted; data shown are the average ± SEM of three independent experiments (n=3). In bar graph, P<0.05 (*), represents the result of paired Student’s t test with 4 degrees of freedom for the corresponding agonist (DA or SKF R-38393) alone-treated group; p<0.05 (#), represents the result of paired Student’s t test with 4 degrees of freedom for the corresponding control group. C. Immunocytochemistry of p-ERK1/2 labeling in striatal neurons up treatment with DA, H2O2 or SKF R-38393. Neuronal cultures were pretreated for 15 min with 1 μM each of either SCH 23390, KT5720 or U0126, or 20 μM of SMBS, prior to the addition of 10 μM of either DA, H2O2, SKF R-38393, or vehicle (0.2 % H2O) for 20 min. Immunocytochemical studies were conducted as described in Experimental Procedures. Scale bar, 100 μm.