Both hormonal and neural signals from the gastrointestinal tract are thought to participate in the process of satiation following the ingestion of food. The fact that chemical and mechanical stimulation of the digestive tract release peptide hormones and activate viscerosensory neurons is indisputable. Nevertheless, the role of individual hormones and their interaction with particular chemical or mechanical stimuli involved in the physiological control of ingestion is unclear. Recent work from our laboratory indicates that the gastrointestinal hormone, cholecystkinin (CCK), as well as some gastrointestinal chemical stimuli, suppress food intake by activating small unmyelinated visceral sensory neurons. Furthermore, pharmacological data suggest that the neurons which mediate suppression of feeding in response to injections of exogenous CCK may also be involved in the suppression of feeding by intestinal stimulation of the intestine with specific nutrients. The experiments in this application will utilize a combination of pharmacologic, behavioral and electrophysiological methodologies to determine the relationship between neural substrates which mediate suppression of feeding by the hormone, CCK, and those which mediate suppression of feeding by specific gastrointestinal stimuli. The results will yield increased understanding of how specific putative endocrine and neural satiety signals access and are processed by the nervous system. In addition, the experiments should shed light on the way in which CCK may be involved in the mediation of the behavioral effects of specific gastrointestinal stimuli which suppress feeding and therefore may help to elucidate the role of this peptide and other gastrointestinal stimuli in the control of food intake.
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