Note that it is possible and indeed likely that a facilitation of control switching under L-DOPA works in concert with an enhancement of the model-based system itself. The predominant view in computational and systems neuroscience holds that phasic dopamine underlies model-free behavior by encoding reward prediction errors. On the other hand,

animal and cognitive approaches emphasize Panobinostat a role for dopamine in model-based behavior such as planning and reasoning (Berridge, 2007; Clatworthy et al., 2009; Cools and D’Esposito, 2011; Robbins and Everitt, 2007). Contrasting with interest in the model-free and model-based system separately is the lack of data on the arbitration between these two behavioral controllers. Our experiment fills

this gap by pitting model-free and model-based control against each other in the same task and in so doing provides SP600125 cell line strong evidence for an involvement of dopamine in the arbitration between model-free and model-based control over behavior. Our findings advocate an effect of L-DOPA on the arbitration between model-based and model-free control, without a modulation of the model-free system itself. Note that the majority of studies reporting enhanced or impaired learning under dopaminergic drugs used either Parkinson’s disease (PD) patients (Frank et al., 2004; Voon et al., 2010) or involved agents that primarily act at D2 receptors ADAMTS5 (Cools, 2006; Frank and O’Reilly, 2006). In contrast with these studies, we did not find evidence for any modulation by L-DOPA of model-free learning rates or indeed evidence of impaired model-free choices. These deviations might partly be explained by PD patients’ more severely reduced dopamine availability off their dopamine replacement therapy (in contrast to our placebo condition) and the much

higher doses of medication involved in PD treatment. Consistent with this explanation is that the effect of L-DOPA on instrumental learning in healthy volunteers was found to be significant only when compared to an inhibition of the dopamine system (via haloperidol) but not when compared to placebo (Pessiglione et al., 2006). Our task does not allow us to dissociate between learning and performance effects. Previous work has suggested interactions between model-based and model-free systems during learning. In this framework, reward prediction errors that are in line with model-based predictions are enhanced, while reward prediction errors that are in opposition with model-based predictions are attenuated (confirmation bias) (Biele et al., 2011; Doll et al., 2009, 2011).