Objective Irritable bowel syndrome (IBS) is a common gastrointestinal disorder characterized by abdominal pain and bloating in association with altered bowel movements.However, its pathogenesis and the underlying molecular mechanisms of visceral hyperalgesia remain elusive.We therefore investigated whether adrenergic signaling pathway is involved in visceral hyperalgesia at adult induced by neonatal colonic inflammation (NCI).Methods Visceral hypersensitivity was induced by colonic injection of 0.5% acetic acid (AA, 0.2 mL) in 10-day-old rats.Behavioral response to colorectal distension (CRD) was measured by visual observation of abdominal withdrawal reflex (AWR) by a blinded observer.Results NCI significantly increased the visceromoter response to CRD, which started 6 weeks and returned to normal level 12 weeks after neonatal colonic infusion of AA.Systemic administration of nonselective β-adrenergic receptor antagonist (propranolol) attenuated NCI-induced visceral hypersensitivity in a dose-dependent manner while α-adrenergic receptor antagonist (phentolamine) did not produce any effect in AA-treated rats.Administration of propranolol did not produce any effect on AWR scores in healthy rats, indicating that this agent did not act as a non-specific analgesic and that adrenergic system did not normally participate in the responses to CRD.Conclusion These data suggest that NCI-induced visceral hypersensitivity is mediated, at least in a large part, by β-adrenergic receptors, thus identifying a specific neurobiological target for the treatment of chronic visceral pain.