The Biological Basis of Incremental Learning: Functional Neuroimaging of Reward-Related Processing in Parkinson’s Disease

Julie Fiez, PhD.
Departments of Psychology and Neuroscience, the Center for the Neural Basis of Cognition, and the Learning Research and Development Center
University of Pittsburgh


Neurophysiological and lesion studies have identified the striatum as a critical component of reward-related processing and have determined that dopamine is central to the signaling of rewards in animals. Dr. Fiez and her co-investigators’ objective is to extend this research to humans. In this pilot study, it is hypothesized that the firing of brainstem dopamine neurons underlies the dynamic modulation of striatal activity in humans. Specifically, they aim to investigate how previously observed differences in responses to reward and punishment vary as a function of phasic, but not tonic, dopaminergic modulation and to estimate the effect size of these differences.

To support their hypothesis, individuals with Parkinson’s disease and controls will perform a guessing game task that has previously been shown to modulate striatal activity in response to reward and punishment. This task will be performed in a functional MRI based session. Assessment of Parkinson’s patients will enable them to capitalize on drug manipulations that affect tonic and phasic dopamine release. A within-subjects analysis of Parkinson’s disease subjects who are either off medication, administered levodopa, administered dopamine agonist, or administered levodopa and dopamine agonist will be compared. In addition, a between-group analysis will be conducted in order to establish that Parkinson’s disease patients have a baseline striatal response to rewards and punishments that is below that of age-matched controls.

Based on previous literature, it is predicted that Parkinson’s subjects who are off medication will have a blunted response to reward. It is also predicted that levodopa, which should restore both tonic and phasic dopamine release, will re-establish a normal striatal response to reward and punishment. In contrast, dopamine agonist, which should restore tonic but not phasic dopamine signaling, will fail to alter striatal responses to reward and punishment.


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