The recent development of selective opioid agonists has permitted a better understanding of the importance of the central opioid system in the modulation of propulsion of gastrointestinal contents. It is now apparent that the types of cerebral opioid receptors involved in gut motility are also associated with other opioid effects (e.g. thermal and visceral analgesia). Other types of cerebral opioid receptors are associated with analgesia, but not with gastrointestinal effects. Furthermore, the opioid receptor subtypes in the spinal cord that are involved in these centrally initiated gut effects are not necessarily the same as those at the cerebral level; compounds affecting the gut at spinal cord sites do not always produce similar effects when given into the brain. Spinally-administered opioids do not require communication with supraspinal sites in order to affect the gut. In contrast, bombesin, a nonopioid neuropeptide that normally inhibits transit after intracerebroventricular or intrathecal administration, fails to alter gut motility on intrathecal administration if communication between the brain and the spinal cord has been disrupted. Frank Porreca, James J. Galligan and Thomas F. Burks discuss these developments which indicate that distinct chemosensitive sites within the CNS can be activated to alter gut motility and which offer exciting possibilities for future therapeutic application.
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