Junk food diet-induced obesity increases D2 receptor autoinhibition in the ventral tegmental area and reduces ethanol drinking

Similar to drugs of abuse, the hedonic value of food is mediated, at least in part, by the mesostriatal dopamine (DA) system. Prolonged intake of either high calorie diets or drugs of abuse both lead to a blunting of the DA system. Most studies have focused on DAergic alterations in the striatum, bu...

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Published in:	PloS one Vol. 12; no. 8; p. e0183685
Main Authors:	Cook, Jason B, Hendrickson, Linzy M, Garwood, Grant M, Toungate, Kelsey M, Nania, Christina V, Morikawa, Hitoshi
Format:	Journal Article
Language:	English
Published:	United States Public Library of Science 31-08-2017 Public Library of Science (PLoS)
Subjects:	Adaptation Alcohol Drinking - metabolism Animals Bacon Biology and Life Sciences Breakfast cereals Care and treatment Cereals Chip breakers Chocolate Conditioning Cookies Diet Diet, High-Fat - adverse effects Dopamine Dopamine - metabolism Dopamine D2 receptors Dopamine receptors Dopaminergic Neurons - metabolism Dopaminergic Neurons - pathology Drinking Drinking (Alcoholic beverages) Drinking behavior Drug abuse Drugs Ethanol Ethanol - adverse effects Feeding Food Health aspects Humans Inhibition (Neurophysiology) Junk foods Laboratories Medicine and Health Sciences Mesencephalon Mesencephalon - metabolism Metabolism Neostriatum Neurons Neurosciences Obesity Obesity - etiology Obesity - metabolism Obesity - pathology Physical Sciences Place preference conditioning Potatoes Rats Receptors, Dopamine D2 - metabolism Reinforcement Rodents Sucrose Sugar Ventral Tegmental Area - metabolism Ventral Tegmental Area - pathology Ventral tegmentum United States > US Texas
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Summary:	Similar to drugs of abuse, the hedonic value of food is mediated, at least in part, by the mesostriatal dopamine (DA) system. Prolonged intake of either high calorie diets or drugs of abuse both lead to a blunting of the DA system. Most studies have focused on DAergic alterations in the striatum, but little is known about the effects of high calorie diets on ventral tegmental area (VTA) DA neurons. Since high calorie diets produce addictive-like DAergic adaptations, it is possible these diets may increase addiction susceptibility. However, high calorie diets consistently reduce psychostimulant intake and conditioned place preference in rodents. In contrast, high calorie diets can increase or decrease ethanol drinking, but it is not known how a junk food diet (cafeteria diet) affects ethanol drinking. In the current study, we administered a cafeteria diet consisting of bacon, potato chips, cheesecake, cookies, breakfast cereals, marshmallows, and chocolate candies to male Wistar rats for 3-4 weeks, producing an obese phenotype. Prior cafeteria diet feeding reduced homecage ethanol drinking over 2 weeks of testing, and transiently reduced sucrose and chow intake. Importantly, cafeteria diet had no effect on ethanol metabolism rate or blood ethanol concentrations following 2g/kg ethanol administration. In midbrain slices, we showed that cafeteria diet feeding enhances DA D2 receptor (D2R) autoinhibition in VTA DA neurons. These results show that junk food diet-induced obesity reduces ethanol drinking, and suggest that increased D2R autoinhibition in the VTA may contribute to deficits in DAergic signaling and reward hypofunction observed with obesity.
Bibliography:	Current address: In Vivo Neurobiology Laboratory, Neurobiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America Competing Interests: The authors have declared that no competing interests exist.
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0183685