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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Eur J Neurosci. 2001 Oct;14(7):1113. doi: 10.1046/j.0953-816x.2001.01736.x

Fig. 3.

Fig. 3

Antagonism of capsaicin-evoked iCGRP release from rat buccal mucosa by capsazepine. Freshly dissected buccal mucosa tissue (both sides of the oral cavity of one rat per chamber) was superfused with physiologicic Krebs buffer (pH = 7.4) for 70 min to establish a stable level of basal iCGRP release in the superfusate. Separate groups of chambers (n = 5–6 per group) were either superfused with vehicle (solid bars) or 300 μM capsazepine (open bars) for three fractions with 100 μM capsaicin being cosuperfused during the middle fraction. Data are expressed as mean ± SEM iCGRP release (fmol). Analysis of variance revealed significant main effects for fraction number (F1,10 = 27.98, P < 0.0005) and for antagonist pretreatment (F1,10 = 55.42, P < 0.0001) as well as a significant interaction term (F1,10 = 16.94, P < 0.005). Significantly different from *VEH/CAP Baseline or †VEH/CAP Peak (P < 0.001).