The present thesis examined the potential interaction between postingestive cues and the dopamine antagonist pimozide on the inhibition of sucrose sham intake. Coadministration of CCK and pimozide IP produced additive inhibitory effects on sham feeding of 4% or 17.1% sucrose. Manipulations of blood glucose levels by infusion of 10% dextrose or injection of 0.1U insulin SC did not interact with pimozide to alter the latter drug's inhibition of 34.2% sucrose sham feeding. Separate experiments verified that these manipulations significantly altered blood glucose levels compared to a control 0.9% saline infusion IV. Infusions of d-glucose into the lateral ventricle significantly enhanced the inhibitory effects of pimozide on 34.2% sucrose sham intake compared to infusions of!glucose or 2-deoxy-glucose. Infusions of d-glucose into the third ventricle, however, significantly attenuated the inhibitory effects of pimozide on 34.2% sucrose sham feeding compared to the control l-glucose infusions. These results collectively suggest that some postingestive cues, such as elevations in third ventricle glucose levels, are indeed capable of inhibiting the suppressive effects of pimozide on sucrose sham feeding. / Thesis / Master of Science (MSc)

To test the hypothesis that postprandial rises of plasma glucose attenuate the motivation derived from positive tastes, I analyzed the effects of intraperitoneal (ip) injections of glucose on sham feeding, a preparation in which food intake is motivated primarily by taste sensations. IP glucose suppressed sham feeding, with maximal suppressions approximating 42%, but only when glucose was administered contiguous with oropharyngeal stimulation. The food intake inhibition produced by ip glucose interacted with palatability; smaller doses of glucose were required to suppress less concentrated sucrose solutions. Closing the gastric cannula increased the potency with which ip glucose inhibited eating suggesting synergy of postabsorptive glucose with other postgastric satiety signals. The inhibition of eating produced by ip glucose did not result from malaise. Thus, postabsorptive rises of plasma glucose decrease the ability of taste cues to drive ingestion and suggest that this phenomenon may contribute to spontaneous meal termination. / Thesis / Master of Science (MSc)

<p> The present thesis examined the relative contribution of hypothalamic and nucleus accumbens dopaminergic activity to the control of sucrose sham feeding. Bilateral intracranial infusions of the dopamine antagonist, haloperidol at doses of 1.25, 2.5, 5 and 7.5 ug, into the hypothalamus and nucleus accumbens produced dose-dependent suppressions of sham feeding of a 15% sucrose solution. No differences in temporal pattern of intake were observed between hypothalamic and nucleus accumbens infusions under drug or vehicle conditions. Also, motor deficits were observed with the highest dose of haloperidol (7.5 ug) while the three lower doses inhibited sham feeding without obvious signs of motor impairment. These results suggest that mesolimbic as well as hypothalamic dopaminergic activity mediate the hedonic aspects of feeding. </p> / Thesis / Master of Science (MSc)

Two major aspects of CCK-induced satiety were examined in the food deprived sham-feeding rat: the kinetics of the inhibition of feeding produced by CCK and the interaction of CCK-induced satiety with oropharyngeal stimulation. Four results were presented regarding the kinetics of the CCK satiety effect. First, CCk administered coincident with the initiation of sham feeding inhibits feeding in a dose-related manner. Second, the increased efficacy of the higher dose of CCK delivered at the same time as sham feeding results from an increase in the size of maximum suppression and an increase in the time of suppression effected via a decreased latency to suppression. Third, CCk delivered 15 minutes before sham feeding begins has no effect on feeding. Fourth, the administration of a long-lasting derivative of CCK 15 minutes prior to the initiation of sham feeding can suppress intake. Two results were presented regarding the role of oropharyngeal stimulation in CCK-induced satiety. First, it was shown that oropharyngeal stimulation enhances the satiety action of CCK. Second, the amount and pattern of feeding inhibition produced by CCK are equivalent regardless of whether the peptide is administered coincident with, or some time after, the initiation of sham feeding. The implications of these results for the therapeutic use of this peptide and its role in producing satiety are discussed. / Thesis / Master of Arts (MA)