Gustatory stimuli, particularly those that taste sweet to humans, initiate and maintain ingestive behavior. They also provide reward sufficient to support the learned behavior used by most animals to locate food. Reward mechanisms related to feeding (and other biological drives) have been linked to the mesolimbic dopamine (DA) system in general, and to the nucleus accumbens, specifically. Nevertheless, the function of accumbens DA in reward remains unclear. Taste provides a logical tool for examining central reward mechanisms. Sapid chemicals are quantified easily, they are transduced via a single, well-described sensory channel, and they can be disassociated from their nutritional consequences. Conversely, such testing of the central reward systems can shed light on a central conundrum of gustatory physiology -how the hedonic qualities of tastes can be reconciled with their purely sensory characteristics. Despite the substantial overlap between taste and reward, relatively little experimental attention has been focused on the interaction of these systems at the neural level. The present experiments are designed to: 1) investigate whether sapid sucrose activates the mesoaccumbens DA neurons in a concentration dependent manner during sham feeding; 2) evaluate the effect sucrose licking on NAc DA during chronic weight reduction, as a model of reward sensitization; and 3) examine the contributions of DI and D2 dopaminergic mechanisms of the NAc in the mediation of both the behavioral and neurochemical activation related to sucrose ingestion in both normal and underweight rats. Unlike previous sham-feeding studies that used systemic injections, dopaminergic drugs will be perfused locally in the NAc through reverse microdialysis. The long-term objective of such an investigation is to understand how food-related oral stimuli produce reward. This knowledge is directly relevant to understanding the control of normal ingestive behavior and to the maladies related to this essential behavior, such as obesity, anorexia nervosa, bulimia nervosa, and binge eating disorder.

National Institute of Health (NIH)
National Institute on Deafness and Other Communication Disorders (NIDCD)
Small Research Grants (R03)
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Special Emphasis Panel (ZDC1-SRB-O (23))
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Davis, Barry
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Pennsylvania State University
Schools of Medicine
United States
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Hajnal, Andras; Smith, Gerard P; Norgren, Ralph (2004) Oral sucrose stimulation increases accumbens dopamine in the rat. Am J Physiol Regul Integr Comp Physiol 286:R31-7
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Hajnal, Andras; Norgren, Ralph (2002) Repeated access to sucrose augments dopamine turnover in the nucleus accumbens. Neuroreport 13:2213-6
Hajnal, A; Norgren, R (2001) Accumbens dopamine mechanisms in sucrose intake. Brain Res 904:76-84