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Visceral hypersensitivity is a common feature offunctional bowel disorders, where an increased number ofmast cells have often been described. Thus, weinvestigated the effect of an experimental mast cell degranulation induced by BrX-537A on somatic(tail heating) and visceral (rectal distension)sensitivity in rats and the involvement of histamineand/or serotonin on this last response. After BrX-537Aadministration, the latency of tail withdrawal reflex wasshortened within the 2- to 8-hr period. Moreover,BrX-537A reduced the distension volume threshold from0.8 ml to 0.4 ml inducing allodynia, from 6 to 12 hrafter its administration. This effect was suppressedby doxantrazole (mast cell stabilizing agent) and WAY100635 (5-HT1A receptor antagonist), andreproduced by 5-HTP (5-HT precursor) and 8-OH-DPAT(5-HT1A receptor agonist). However, neither granisetron(5-HT3 receptor antagonist) nor H1, H2, or H3 histaminereceptor antagonists modified the BrX-537A-inducedallodynia. Consequently, mast cell degranulation initiates a delayed somatic and visceralallodynia, with the participation of serotonin, through5-HT1A receptor activation, on the visceralresponse.