Treatments | SERT activity (% control) | Percentage of inhibition |
---|---|---|
Vehicle | 100.00 ± 0.05 | 0.00 |
PD169316 | 64.78 ± 3.00 | 35.22a |
β-PMA | 74.95 ± 2.16 | 25.05a |
PD169316 plus β-PMA | 47.16 ± 1.98 | 52.84a,b |
Staurosporine | 97.26 ± 3.90 | 2.74c |
Staurosporine plus PD169316 | 59.78 ± 3.30 | 40.22a |
Staurosporine plus β-PMA | 98.01 ± 2.64 | 1.99c |
Staurosporine plus PD169316 plus β-PMA | 63.95 ± 3.16 | 36.05a,d |
BIM I | 102.26 ± 1.25 | 0.00c |
BIM I plus PD169316 | 53.78 ± 1.29 | 46.22a |
BIM I plus β-PMA | 102.99 ± 5.84 | 0.00c |
BIM I plus PD169316 plus β-PMA | 69.05 ± 4.23 | 30.95a,d |
Purified rat midbrain synaptosomes were preincubated for 30 min at 37°C in the absence (vehicle) or presence of the following agents: PD169316, 10 μm; β-PMA, 1 μm; bisindolylmaleimide I, 500 nm; and staurosporine, 2.5 μm. Protein kinase C inhibitor staurosporine and BIM I were added 20 min before the addition of PD169316, β-PMA, or both. 5-HT uptake was performed as described in Materials and Methods. Experiments were conducted in triplicate, and the mean values ± SEM from three independent experiments are given. Significant differences were determined by one-way ANOVA with a Tukey-Kramer post hoc test.
↵ a Significantly different from levels observed under vehicle conditions; p < 0.01.
↵ b Significantly different from the levels observed with the application of single modulator (PD169316 or β-PMA); p < 0.05.
↵ c Not statistically different from the levels observed under vehicle conditions.
↵ d Significantly different from the levels observed with coapplication of PD169316 and β-PMA; p < 0.05.