47 / 218
45
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.