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Irritable bowel syndrome (IBS) is a disorder of unknown etiology characterized by widespread, chronic abdominal pain associated with altered bowel movements. Increasing amounts of evidence indicate that stressors presented during gestational periods could have long-term effects on the offspring's tissue structure and function, which may predispose to gastrointestinal diseases. The aim of the present study is designed to determine whether prenatal maternal stress (PMS) is a adverse factor affecting gastrointestinal sensitivity and to investigate possible mechanisms underlying PMS-induced visceral hypersensitivity in adult offspring. PMS was induced in pregnant Sprague Dawley rats by exposure to heterotypic intermitent stress from gestational day 7 to delivery. PMS significantly increased visceromotor response to colorectal distention (CRD) in adult offspring from the age of 6 weeks to 10 weeks. PMS also enhanced neuronal excitability including depolarization of resting membrane potentials, reduction in rheobase and an increase in the number of action potentials evoked by 2X and 3X rheobase current stimultion of colon-specific dorsal root ganglion (DRG) neurons. PMS remarkably enhanced expression of cystathionine-β-synthase (CBS) and Nav1.7 in T13-L2 thoracolumbar DRGs both at protein and mRNA levels. Intraperitoneal injected of AOAA, an inhibitor of CBS, attenuated PMS-induced visceral hypersensitivity in a dose dependent manner. A consecutive 7 day administration of AOAA reversed the hyperexcitability of colon-specific DRG neuorns and markedly reduced Nav1.7 expression. These results indicate that the presence of multiple psychophysical stressors during pregnancy is associated with visceral hypersensitivity in offspring, which is likely mediated by an upregualtion of CBS and Nav1.7 expression. PMS might be a significant contributor to IBS and CBS might be a potential target for treatment for chronic visceral hypersensitivity in patients with IBS.

molecular pain

Prenatal maternal stress induces visceral hypersensitivity of adult rat offspring through activation of cystathionine-<b>β</b>-synthase signaling in primary sensory neurons

Prenatal maternal stress induces visceral hypersensitivity of adult rat offspring through activation of cystathionine-β-synthase signaling in primary sensory neurons