S ince 1970, a large number of brain peptides have been characterized using techniques of biochemistry, immunohistochemistry, and molecular biology. The identification of these peptides led to an explosion of knowledge of their distribution and biological actions in the central nervous system (CNS) and spinal cord. In particular, the combined use of immunohistochemical and retrograde tracing techniques showed that brain nuclei influencing gut motor function contain a variety of peptides (l-4). A decade ago, pioneer neuropharmacological observations by Smith et al.(5), Burks (6). and Bu&no et al.(7) demonstrated that the brain is a target site of action for peptides that alter gastrointestinal (GI) motor function. Since then, investigations have unraveled both brain sites of action and neurohumoral pathways mediating their effects. At least 12 peptides act in the brain to alter GI contractile activity and transit in rodents, cats, rabbits, or dogs. However, the understanding of their physiological role is still limited. Several factors contribute to this lack of information. For most neuropeptides, specific blocking agents are not available and their endogenous brain release in response to physiological events is difficult to assess. Moreover, many experiments in rodents are performed under anesthesia and involve acute surgical preparation to monitor motility. While these studies provide valuable information about central nervous structures and pathways impinging on GI motor function, they cannot be interpreted in terms of normal physiology.

This article will review peptides established to act in the brain to influence GI motility and transit in experimental animals. Peptide action will be discussed in relation to the alterations of the characteristic pattern of contractile activity in the fasted or fed state in conscious or anesthetized animals. The sequence of peptide grouping is based on the amount of information available on each peptide and how it