Figure 3
From: Rapid S-nitrosylation of actin by NO-generating donors and in inflammatory pain model mice
No mediation of the cGMP/PKG pathway in inhibition of dopamine release by NOR1. A. Effect of membrane-permeable cGMP and cAMP analogues on PACAP-stimulated dopamine release. PC12 cells (4 × 105 cells/well) cultured on 24-well dishes were stimulated for 10 min with 10 nM PACAP and 100 μM NOR1, 8-Br-cAMP or 8-Br-cGMP in the absence or presence of 100 μM IBMX. **P < 0.01 vs. none; ##P < 0.01 vs. IBMX. B. Effect of inhibitors of the cGMP/PKG pathway on PACAP-stimulated dopamine release by NOR1. PC12 cells were preincubated for 30 min with 100 μM NOR1 and 300 nM ODQ or 1 μM KT5823 in the presence of 10 μM imipramine. Then the cells were stimulated for 5 min by the addition of 10 nM PACAP. **P < 0.01 vs. PACAP alone (none). C. Effect of inhibitors of the cGMP/PKG pathway on basal dopamine release. PC12 cells were incubated for 5 min with 1 μM KT5823 or 1 μM glibenclamide without or with 100 μM NOR1. Dopamine was measured by HPLC, and dopamine released into the medium (mean ± SD, n = 3) was expressed as a percentage of total dopamine in PC12 cells, as described in "Methods." **P < 0.01 vs. none.