Inflammatory bowel disease (IBD) is associated with inflammatory activity in the GI tract and birth complications in pregnant women. The long-term impact of gestational IBD on offspring development, however, has not been examined. Here, we employed dextran sulfate sodium (DSS, 2.5% in drinking water on GD9-12) to induce colonic mucosa ulceration to the pregnant C57BL/6 mice dams. Offspring from DSS-treated dams were compared with non-treated dams at juvenile (PND 30) and adult age (PND 70) in behavioural tests sensitive to the acute gestational infection induced by polyinosinic:polycytidylic acid (Poly I:C). Prenatal DSS treatment impaired sensorimotor gating in the prepulse inhibition (PPI) paradigm, and hippocampus-dependent memory in the Y-maze test of spatial familiarity judgement. The PPI deficit did not emerge until adulthood, resembling the age-dependency of PPI deficit reported in the Poly I:C model of maternal infection. By contrast, the Y-maze deficit was only observed in juvenile age but no longer present in adulthood. The age dependency of this memory deficit has not been observed in the Poly I:C model and may suggest a transient delay in the maturation of the hippocampus-dependent memory system. Both age-dependent behavioural modifications were observed in male as well as female offspring from DSS-treated dams. While our study has added to evidence that early life development is vulnerable to physiological disturbances of the maternal host during gestation, we also showed that the consequence of our gestational IBD model on behavioural development in the offspring can be readily distinguished from model of gestational infection-like immune disturbances.