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Eur J Neurosci. 2019 Jul 23. doi: 10.1111/ejn.14527. [Epub ahead of print]

Recruitment and disruption of ventral pallidal cue encoding during alcohol seeking.

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Solomon H. Snyder Department of Neuroscience, Johns Hopkins School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Department of Psychological and Brain Sciences, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD, USA.
Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD, USA.
Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA.


A critical area of inquiry in the neurobiology of alcohol abuse is the mechanism by which cues gain the ability to elicit alcohol use. Previously, we found that cue-evoked activity in rat ventral pallidum robustly encodes the value of sucrose cues trained under both Pavlovian and instrumental contingencies, despite a stronger relationship between cue-evoked activity and behavioral latency after instrumental training (Richard et al., 2018, Elife, 7, e33107). Here, we assessed: (a) ventral pallidal representations of Pavlovian versus instrumental cues trained with alcohol reward, and (b) the impact of non-associative alcohol exposure on ventral pallidal representations of sucrose cues. Decoding of cue identity based on ventral pallidum firing was blunted for the Pavlovian alcohol cue in comparison to both the instrumental cue trained with alcohol and either cue type trained with sucrose. Further, non-associative alcohol exposure had opposing effects on ventral pallidal encoding of sucrose cues trained on instrumental versus Pavlovian associations, enhancing decoding accuracy for an instrumental discriminative stimulus and reducing decoding accuracy for a Pavlovian conditioned stimulus. These findings suggest that alcohol exposure can drive biased engagement of specific reward-related signals in the ventral pallidum.


alcohol exposure; associative learning; decoding; electrophysiology; reward


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