Figure 3. Effects of EP2 and EP3 agonists in trigeminal sensory neurons. (A) Cultured trigeminal ganglia neurons were exposed to either vehicle or butaprost (1 µM and 10 µM, 15 min) or sulprostone (1 µM and 10 µM, 15 min), and the supernatant was collected for measurement of the amount of iCGRP by radioimmunoassay [n = 6–18 wells per condition; data presented as % of basal release (mean ± SEM); *** = p < 0.001; butaprost- and sulprostone-evoked release was compared with the vehicle treatment by one-way ANOVA with the Bonferroni post hoc test]. (B) Cultured trigeminal ganglia neurons were exposed to either vehicle, butaprost (10 µM), or PGE₂ (1 µM) for 15 min, and the supernatant was removed. The neurons were then exposed to capsaicin (30 nM, 15 min), and the supernatant was measured for amount of iCGRP [n = 6 wells per condition; data presented as % of basal release (mean ± SEM); *p < 0.05, **p < 0.01; capsaicin-evoked release following either PGE₂ or butaprost pre-treatment was compared with vehicle pre-treatment by one-way ANOVA with the Bonferroni post hoc test].