For example, opioid receptor stimulation in a posterior VP “hedonic hotspot” causes increases in the number of hedonic “liking” reactions elicited by sucrose taste ( Smith and Berridge 2005). 2006 Skoubis and Maidment 2003 Smith and Berridge 2005 Tang et al. Indeed, the VP mediates reward in the sense that direct manipulations of the VP cause changes in the hedonic impact of sweet tastes and reward value of other incentives ( June et al. 2004), suggesting that positive hedonic signals might be encoded in neural firing rates. Sucrose rewards elicit increased firing in VP neurons in rats ( Tindell et al. How are hedonic impact reversals coded in the brain? The ventral pallidum (VP) is an especially likely candidate to code sensory pleasure because it receives converging inputs from gustatory circuits and limbic circuits that mediate natural and drug rewards ( Kalivas et al. 2005 Leshem and Rudoy 1997 Richter 1936 Roitman et al. 1984 Clark and Bernstein 2004, 2006 Kochli et al. For example, physiological sodium depletion reverses “disliking” reactions to hypertonic NaCl taste into “liking” reactions in rats (e.g., tongue protrusions) and increases the perceived pleasantness of salt for humans ( Beauchamp et al. However, even the unpleasant valence of intense salty tastes can be reversed from negative to positive by physiological sodium deficiency states, in a hedonic phenomenon called taste “alliesthesia” ( Cabanac 1971). Ordinarily, hypertonic concentrations of NaCl (such as seawater) taste unpleasant to humans and elicit “disliking” gape reactions from rats (although lower concentrations of salt are often pleasant) ( Schulkin 1993 Stellar 1980). Salt is crucial to survival and can be a potent hedonic stimulus. 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. In summary, VP firing activity selectively tracks the hedonic values of tastes, even across hedonic reversals caused by physiological changes. By contrast, VP neural activity to “liked” sucrose taste was always high and never altered. 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. We also compared firing elicited by palatable sucrose taste, which always elicited “liking” reactions in both states. 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. 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. The ventral pallidum (VP) is a key structure in brain mesocorticolimbic reward circuits that mediate “liking” reactions to sensory pleasures.
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