Fig. 2
The PGE2-induced increase of capsaicin-evoked iCGRP release from sensory neurons is attenuated by H-89 after acute exposure to the eicosanoid but not after long-term exposure. a, b Each column represents the mean ± SEM of iCGRP release as percent of total iCGRP content per well of cells maintained in the absence of added NGF. Lightly shaded columns indicate basal release whereas dark-shaded columns represent capsaicin-stimulated release of iCGRP. Cultures were treated with vehicle (a) or 1 μM PGE2 (b) for 5 days and then washed and acutely exposed to 1 μM PGE2 for 20 min in the absence or presence of 10 μM H-89, as indicated. An asterisk indicates a statistically significant difference between capsaicin-stimulated iCGRP release after exposure to vehicle versus after a 10-min exposure to PGE2 (1 μM) using one-way ANOVA followed by Bonferroni’s post hoc test. c Each column represents the mean ± SEM of cAMP content. The left panel represents cAMP content from cells exposed to vehicle for 5 days, whereas the right panel represents cAMP content from cells exposed to PGE2 (1 μM) for 5 days. Cultures were washed and then re-exposed for 10 min to vehicle (open columns), 1 μM PGE2 (light gray columns), or 1 μM forskolin (dark gray columns). An asterisk indicates a statistically significant difference from vehicle using one-way ANOVA followed by Bonferroni’s post hoc test