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J Neurophysiol 96: 2399-2409, 2006. First published August 2, 2006; doi:10.1152/jn.00576.2006
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Ventral Pallidum Firing Codes Hedonic Reward: When a Bad Taste Turns Good

Amy J. Tindell1, Kyle S. Smith1, Susana Peciña1, Kent C. Berridge1 and J. Wayne Aldridge1,2

1Department of Psychology University of Michigan; and 2Department of Neurology, University of Michigan Medical School, Ann Arbor, Michigan

Submitted 2 June 2006; accepted in final form 26 July 2006

The ventral pallidum (VP) is a key structure in brain mesocorticolimbic reward circuits that mediate "liking" reactions to sensory pleasures. Do firing patterns in VP actually code sensory pleasure? Strong evidence for hedonic coding requires showing that neural signals track positive increases in sensory pleasure or even reversals from bad to good. A useful test is the salt alliesthesia of physiological sodium depletion that makes even aversively intense NaCl taste become palatable and "liked." We compared VP neural firing activity in rats during aversive "disliking" reactions elicited by a noxiously intense NaCl taste (triple-seawater 1.5 M concentration) in normal homeostatic state versus in a physiological salt appetite state that made the same NaCl taste palatable and elicit positive "liking" reactions. We also compared firing elicited by palatable sucrose taste, which always elicited "liking" reactions in both states. A dramatic doubling in the amplitude of VP neural firing peaks to NaCl was caused by salt appetite that matched the affective switch from aversive ("disliking") to positive hedonic ("liking") reactions. By contrast, VP neural activity to "liked" sucrose taste was always high and never altered. In summary, VP firing activity selectively tracks the hedonic values of tastes, even across hedonic reversals caused by physiological changes. Our data provide the strongest evidence yet for neural hedonic coding of natural sensory pleasures and suggest, by extension, how abnormalities in VP firing patterns might contribute to clinical hedonic dysfunctions.


Address for reprint requests and other correspondence: J. W. Aldridge, Department of Neurology, University of Michigan Medical School, 1150 West Medical Center Drive, Medical Science Bldg I, Room 3317, Ann Arbor, MI 48109-0607 (E-mail: jwaynea{at}umich.edu)




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