The presence of dopamine-containing neurons in the enteric nervous system has been described, but it is far to be clear their role in the modulation of gut motility. Moreover, ontogenetic studies shows that dopaminergic neurons are late-developing neurons, arising perinatally, but there are no informations if dopaminergic signaling may undergo to developmental changes after birth, as demonstrated for other signaling. Thus, using a pharmacological approach, we examined, in vitro, the role of dopaminergic neurons in the regulation of duodenal contractility in neonatal mice (<=48 h postnatal) compared to the adults. Transcripts for all dopaminergic receptors were detected in mouse duodenum at each age. In postnatal duodenal preparations, dopamine induced a concentration-dependent contraction, reduced by SCH 23390, D₁ receptor antagonist, but not affected by domperidone, D₂ receptor antagonist. Indeed in the preparations from adult mice, dopamine response switch in a concentration-dependent relaxation reduced by domperidone, and, to a lesser extent, by SCH 23390. These data suggest that in the mouse gut, in postnatal period D₁ receptors are exclusively involved in dopamine effects, which undergo to postnatal changes with a shift of the effects from a contractile to a relaxation response. In addition, developmental changes in the levels and pattern of receptor functionality is observed, being in adult mice increased the contribution of D₂ receptors in the dopamine effects.