Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 22, Issue 10, Pages 2617-2634Publisher
WILEY
DOI: 10.1111/j.1460-9568.2005.04411.x
Keywords
addiction; amphetamine sensitization; incentive salience; neural coding; single-unit activity; Sprague-Dawley rat
Categories
Funding
- NIDA NIH HHS [DA017752, DA015188] Funding Source: Medline
- NIMH NIH HHS [MH63649] Funding Source: Medline
- NINDS NIH HHS [NS31650] Funding Source: Medline
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Neurons in ventral pallidum fire to reward and its predictive cues. We tested mesolimbic activation effects on neural reward coding. Rats learned that a Pavlovian conditioned stimulus (CS+1 tone) predicted a second conditioned stimulus (CS+2 feeder click) followed by an unconditioned stimulus (UCS sucrose reward). Some rats were sensitized to amphetamine after training. Electrophysiological activity of ventral pallidal neurons to stimuli was later recorded under the influence of vehicle or acute amphetamine injection. Both sensitization and acute amphetamine increased ventral pallidum firing at CS+2 (population code and rate code). There were no changes at CS+1 and minimal changes to UCS. With a new 'Profile Analysis', we show that mesolimbic activation by sensitization/amphetamine incrementally shifted neuronal firing profiles away from prediction signal coding (maximal at CS+1) and toward incentive coding (maximal at CS+2), without changing hedonic impact coding (maximal at UCS). This pattern suggests mesolimbic activation specifically amplifies a motivational transform of CS+ predictive information into incentive salience coded by ventral pallidal neurons. Our results support incentive-sensitization predictions and suggest why cues temporally proximal to drug presentation may precipitate cue-triggered relapse in human addicts.
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