This investigation evaluated the role of capsaicin-sensitive afferent neurons in the gastroprotective effect of α- and β-amyrin, a triterpenoid mixture isolated from Protium heptaphyllum resin. Gastric mucosal damage was induced in mice by intragastric ethanol and assessed by planimetry. Mice pretreated orally with the amyrin mixture (50 and 100 mg/kg) or capsaicin (2.5 and 5 mg/kg), the pungent principle from red hot peppers, showed a significantly lower intensity of ethanol-associated gastric mucosal damage, in relation to vehicle-treated controls. At higher doses both these agents produced either a diminished protection or no significant effect. The maximal gastroprotection that was observed at the dose of 100 mg/kg amyrin mixture was almost abolished in mice with their sensory afferents chemically ablated by a neurotoxic dose of capsaicin, suggesting that the gastroprotective mechanism of α- and β-amyrin mixture involves at least in part the activation of capsaicin-sensitive primary afferent neurons.