The goal of my research is to understand how individual neurons and neuronal circuits in the basal ganglia contribute and process information related to movement and rewards. I use a combination of tools including: electrophysiology, behavioral manipulation, anatomical techniques, and pharmacology to explore functional neural mechanisms. Our methods are designed to evaluate the pattern and timing of neural activity in relation to behavioral events such as rewards, cues that predict rewards, and to learned and instinctive movements. Our principal method is to record electrical activity of individual nerve cells while animals behave freely. Experimental manipulations include: Pavlovian and instrumental training, diminished or boosted motivational drive states (e.g., diuretic salt depletion), mesolimbic activation (via sensitization and acute injections), and pharmacological stimulation (via systemic and intracranial injections of neurotransmitter agonists and antagonists). I have been funded (by NIH and private foundations) to conduct behavioral neurophysiological research at the University of Michigan since 1982.
Sensory cues associated with rewards gain access to the same neural circuits as primary rewards, and evoke motivational states in a similar manner as primary rewards. Thus, characterizing how the incentive motivational properties of reward cues are represented in the nervous system is crucial to understanding how they come to control behavior, and potentially promote maladaptive behavior, including drug addiction. Although cues associated with food and drug rewards have predictive value, the degree to which cues have incentive value varies between individuals. It is important to understand this property as compulsive disorders such as drug addiction may depend on its influence. Some people have difficulty remaining abstinent in the presence of people, places, and other cues associated with drug-taking. Other individuals can use drugs casually without addiction. We are modeling these individual trait differences in rodents using their behavioral responses to food cues. We are investigating cue-evoked changes in brain activity in ventral reward regions of the basal ganglia (the nucleus accumbens [NAcc] and ventral pallidum [VP]) related to both food and drug cues. By studying individual variation in the attribution of incentive value, we will be able to delineate what aspects (i.e., predictive or incentive properties) of these cues are processed, and whether their neural representations are altered by abused drugs.
Tindell AJ, Berridge KC, Zhang J, Pecina S, Aldridge JW. (2005) Ventral pallidal neurons code incentive motivation: amplification by mesolimbic sensitization and amphetamine. Eur. J. Neurosci. 22: 2617-34. PM:16307604
Tindell AJ, Smith KS, Pecina S, Berridge KC, Aldridge JW. (2006) Ventral pallidum firing codes hedonic reward: when a bad taste turns good. J. Neurophysiol. 96: 2399-409. PMID: 16885520
Berridge KC, Robinson TE, Aldridge, J.W. Dissecting components of reward: 'liking', 'wanting', and learning. Current Opinion in Pharmacology, 9, 65-73, 2009. PMCID: PMC2756052
Zhang J, Berridge KC, Tindell AJ, Smith KS, Aldridge JW. (2008) Modeling the neural computation of incentive salience. 2009; PLoS Computational Biology. 2009; 5(7), e1000437 PMCID: PMC2703828
Tindell AJ, Smith KS, Berridge KC, Aldridge JW. Neural representation of incentive salience in ventral pallidum: wanting what was never liked. J. Neurosci. 2009; 29, 12220-12228 PMCID: PMC2792765 [Available on 2010/3/30]