Table 1.

Specificity and coordinate effects of PD169616- and β -PMA-induced inhibition of SERT activity in rat midbrain synaptosomes

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.