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Chapter 8
reward motivation can indeed have opposite effects on cognitive stability and focussing.
In
chapter 7
we provided evidence for prefrontal modulation of processing in the striatum
during reward processing and the integration of reward, cognition and action. This design
did now allow the testing of the exact nature of these projections. First, we cannot exclude
that information is transferred directly from the anterior prefrontal cortex to the putamen
(or the anterior caudate nucleus to the putamen), thereby bypassing the ‘cognitive’ striatum.
The new rodent paradigm developed in
chapter 6
, with the addition of an action component
(i.e. response switching as in
chapter 7
), allows further testing of this hypothesis. Using a
disconnection approach, lesions of the ventral striatum and of the dorsal contralateral
striatum (which leave intact one ventral striatum and one dorsal striatum in each hemisphere)
(Belin and Everitt, 2008), can be used to assess whether connections between the ventral
striatum and dorsal striatum are crucial for the integration between motivation, cognition
and action. Also, lesions (or stimulation) of the midbrain neurons that project to the dorsal
striatum should affect motivated cognition if the SNS account is valid. Finally, the idea that
serial connections from the ventromedial to increasingly dorsal regions of the striatum, via
dopaminergic midbrain connections (Ikeda et al., 2013), mediate motivated cognitive control
should be substantiated. This can be achieved by showing that the effects of inhibition of the
‘reward cortex’ and ‘reward striatum’ on processing in the ‘motor striatum’ (
chapter 7
) can be
blocked after dopamine receptor antagonism in the ‘cognitive striatum’ (
limitations
).