Mast cell degranulation induces delayed rectal allodynia in rats - Role of histamine and 5-HT

Visceral hypersensitivity is a common feature of functional bowel disorders, where an increased number of mast cells have often been described. Thus, we investigated 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 histamine and/or serotonin on this last response. After BrX-537A administration, the latency of tail withdrawal reflex was shortened within the 2- to 8-hr period. Moreover, BrX-537A reduced the distension volume threshold from 0.8 ml to 0.4 ml inducing allodynia, from 6 to 12 hr after its administration. This effect was suppressed by doxantrazole (mast cell stabilizing agent) and WAY 100635 (5-HT(1A) receptor antagonist), and reproduced by 5-HTP (5-HT precursor) and 8-OH-DPAT (5-HT(1A) receptor agonist). However, neither granisetron (5-HT(3) receptor antagonist) nor H(1), H(2), or H(3) histamine receptor antagonists modified the BrX-537A-induced allodynia. Consequently, mast cell degranulation initiates a delayed somatic and visceral allodynia, with the participation of serotonin, through 5-HT(1A) receptor activation, on the visceral response.