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The Neural Substrates of Reward Processing in Humans: The Modern Role of fMRI
Samuel M. McClure
Human Neuroimaging Lab, Center for Theoretical Neuroscience, Division of Neuroscience, Baylor College of Medicine, Houston, Texas, Department of Psychology, Princeton University, Princeton, New Jersey, smcclure{at}princeton.edu
Michele K. York
Department of Neurosurgery, Baylor College of Medicine, Houston, Texas
P. Read Montague
Human Neuroimaging Lab, Center for Theoretical Neuroscience, Division of Neuroscience, Baylor College of Medicine, Houston, Texas
Experimental work in animals has identified numerous neural structures involved in reward processing and reward-dependent learning. Until recently, this work provided the primary basis for speculations about the neural substrates of human reward processing. The widespread use of neuroimaging technology has changed this situation dramatically over the past decade through the use of PET and fMRI. Here, the authors focus on the role played by fMRI studies, where recent work has replicated the animal results in human subjects and has extended the view of putative reward-processing neural structures. In particular, fMRI work has identified a set of reward-related brain structures including the orbitofrontal cortex, amygdala, ventral striatum, and medial prefrontal cortex. Moreover, the human experiments have probed the dependence of human reward responses on learned expectations, context, timing, and the reward dimension. Current experiments aim to assess the function of human reward-processing structures to determine how they allow us to predict, assess, and act in response to rewards. The authors review current accomplishments in the study of human reward processing and focus their discussion on explanations directed particularly at the role played by the ventral striatum. They discuss how these findings may contribute to a better understanding of deficits associated with Parkinson’s disease.
Key Words: Reward • fMRI • Atriatum • Amygdala • Orbitofrontal cortex • Parkinson’s disease
The Neuroscientist, Vol. 10, No. 3,
260-268 (2004)
DOI: 10.1177/1073858404263526
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