Fig. 2.

Involvement of the cAMP/PKA pathway in depolarization-evoked [³H]-GABA release from rat globus pallidus synaptosomes. a Illustration of a representative experiment. Labeled synaptosomes were perfused with Krebs-Ringer-Hepes solution and [³H]-GABA release was evoked by raising the K⁺ concentration from 4 to 20 mM for the periods indicated by the vertical gray bars. Drugs under test were present for the period indicated by the open bar. Values are expressed as a percentage of [³H]-GABA release in fraction 1 and represent means ± SEM from four to six replicates. b Forskolin and 8-Br-cAMP enhance depolarization-evoked [³H]-GABA release. After subtraction of basal release, the area under the release curves for fractions 3–8 (S1) and 12–17 (S2) was determined for each individual chamber and the ratio S2/S1 was calculated. Values are expressed as a percentage of control [³H]-GABA release (no drugs added) and are means ± SEM from three experiments with four to six replicates. The statistical analysis was performed with ANOVA and Dunnett’s test. c The PKA antagonist H-89 (10 μM) prevented the facilitatory effect of the A_2AR agonist CGS-21680 (3 nM) on K⁺-evoked [³H]-GABA release. Values are means ± SEM from four experiments. d The H₃R agonist immepip (100 nM) did not inhibit the facilitatory effect of 8-Br-cAMP (500 μM) on depolarization-evoked [³H]-GABA release. Values are means ± SEM from five experiments. For panels b and c, the statistical analysis was performed with ANOVA and Dunnett’s test; ns, no significantly different, *P < 0.05, **P < 0.01 versus control values. For panel d, values were compared with ANOVA and Tukey’s test; ns, no significantly different, *P < 0.05