Endogenous opioid peptides derive from three precursors: proenkephalin A, maturing into enkephalins, proenkephalin B, maturing into dynorphins, and proopiomelanocortin, maturing into beta-endorphin and non-opioid fragments. All these opioid peptides can be detected by immunocytochemical methods in many neurons intrinsic to the gut and in cerebral and medullary neurons. The involvement of opioid peptides in the control of intestinal motility is demonstrated by experiments using injection of exogenous peptides or analogues, administration of antagonists or inhibition of their in vivo degradation. However, the pattern of action of opioids on intestinal motility is complex, since stimulant and inhibitory effects may occur via the different mu, delta and kappa opioid receptors, on muscle cells or on nerves and at central or peripheral sites. On the whole, opioid peptides should be considered as important neurotransmitters. Their main function on gut motility seems to be the regulation of other stimulant and inhibitory neurons inputting to the muscle cells of the gut.