Proefschrift_Holstein

General introduction

In summary, genetic imaging work and work in patients with Parkinson’s disease ( chapter 1 ) has suggested a role for striatal dopamine in motivated cognitive control. A role for the dopamine D2 receptor in flexible updating of task demands has been suggested while reward processing has been associated with both dopamine D1 and D2 receptor signalling. In addition, inter-individual differences in response to pharmacological manipulations can be explained by taking into account the baseline state of the dopamine system. The role of specific dopamine receptor-types in motivated cognitive control has thus far not been assessed, nor have dopamine or the striatum been directly manipulated to assess their role in motivated cognitive control. One way by which reward may influence motivated cognitive control is by modulating the mechanism by which the prefrontal cortex and striatum communicate. The work presented in this thesis aimed to address three primary questions. First, it aims to elucidate which specific dopamine receptor is involved inmotivated cognitive control. Second, the role of the striatum is further assessed by directly manipulating the striatum and testing whether it is crucial for motivated cognitive control. Third, I aimed to provide evidence for the idea that prefrontal modulation can change striatal processing during motivated cognitive control. Finally, in chapter 8 I will recap the results and provide an interpretation of the finding presented in this thesis. In short, the aim of the studies presented in this thesis was to increase our understanding of the neural mechanisms that allow prospective rewards to alter our ability to exert cognitive control. More specifically, the experiments in this thesis aim to elucidate the role for striatal dopamine and the corticostriatal network during the integration of reward and flexible cognitive control.

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