A neuronal mechanism underlying decision-making deficits during hyperdopaminergic states

Jeroen P. H. Verharen, Johannes W. de Jong, Theresia J. M. Roelofs, Christiaan F. M. Huffels, Ruud van Zessen, Mieneke C. M. Luijendijk, Ralph Hamelink, Ingo Willuhn, Hanneke E. M. den Ouden, Geoffrey van der Plasse, Roger A. H. Adan () and Louk J. M. J. Vanderschuren ()
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Jeroen P. H. Verharen: University Medical Center Utrecht
Johannes W. de Jong: University Medical Center Utrecht
Theresia J. M. Roelofs: University Medical Center Utrecht
Christiaan F. M. Huffels: University Medical Center Utrecht
Ruud van Zessen: University Medical Center Utrecht
Mieneke C. M. Luijendijk: University Medical Center Utrecht
Ralph Hamelink: Institute of the Royal Netherlands Academy of Arts and Sciences
Ingo Willuhn: Institute of the Royal Netherlands Academy of Arts and Sciences
Hanneke E. M. den Ouden: Radboud University
Geoffrey van der Plasse: University Medical Center Utrecht
Roger A. H. Adan: University Medical Center Utrecht
Louk J. M. J. Vanderschuren: Utrecht University

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Hyperdopaminergic states in mental disorders are associated with disruptive deficits in decision making. However, the precise contribution of topographically distinct mesencephalic dopamine pathways to decision-making processes remains elusive. Here we show, using a multidisciplinary approach, how hyperactivity of ascending projections from the ventral tegmental area (VTA) contributes to impaired flexible decision making in rats. Activation of the VTA–nucleus accumbens pathway leads to insensitivity to loss and punishment due to impaired processing of negative reward prediction errors. In contrast, activation of the VTA–prefrontal cortex pathway promotes risky decision making without affecting the ability to choose the economically most beneficial option. Together, these findings show how malfunction of ascending VTA projections affects value-based decision making, suggesting a potential mechanism through which increased forebrain dopamine signaling leads to aberrant behavior, as is seen in substance abuse, mania, and after dopamine replacement therapy in Parkinson’s disease.

Date: 2018
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DOI: 10.1038/s41467-018-03087-1

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