Striatal Dopamine and Reward Prediction Error Signaling in Unmedicated Schizophrenia Patients

Author:

Katthagen Teresa1,Kaminski Jakob123,Heinz Andreas124,Buchert Ralph5,Schlagenhauf Florian136

Affiliation:

1. Department of Psychiatry and Psychotherapy, Charité Campus Mitte, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

2. Berlin Institute of Health, Berlin, Germany

3. Max-Planck-Institute for Human Cognitive and Brain Sciences, Leipzig, Germany

4. Cluster of Excellence NeuroCure, Charité-Universitätsmedizin, Berlin, Germany

5. Department of Diagnostic and Interventional Radiology and Nuclear Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

6. Bernstein Center for Computational Neuroscience, Berlin, Germany

Abstract

Abstract Increased striatal dopamine synthesis capacity has consistently been reported in patients with schizophrenia. However, the mechanism translating this into behavior and symptoms remains unclear. It has been proposed that heightened striatal dopamine may blunt dopaminergic reward prediction error signaling during reinforcement learning. In this study, we investigated striatal dopamine synthesis capacity, reward prediction errors, and their association in unmedicated schizophrenia patients (n = 19) and healthy controls (n = 23). They took part in FDOPA-PET and underwent functional magnetic resonance imaging (fMRI) scanning, where they performed a reversal-learning paradigm. The groups were compared regarding dopamine synthesis capacity (Kicer), fMRI neural prediction error signals, and the correlation of both. Patients did not differ from controls with respect to striatal Kicer. Taking into account, comorbid alcohol abuse revealed that patients without such abuse showed elevated Kicer in the associative striatum, while those with abuse did not differ from controls. Comparing all patients to controls, patients performed worse during reversal learning and displayed reduced prediction error signaling in the ventral striatum. In controls, Kicer in the limbic striatum correlated with higher reward prediction error signaling, while there was no significant association in patients. Kicer in the associative striatum correlated with higher positive symptoms and blunted reward prediction error signaling was associated with negative symptoms. Our results suggest a dissociation between striatal subregions and symptom domains, with elevated dopamine synthesis capacity in the associative striatum contributing to positive symptoms while blunted prediction error signaling in the ventral striatum related to negative symptoms.

Funder

Deutsche Forschungsgemeinschaft

Berlin Institute of Health

Bundesministerium für Bildung und Forschung

Publisher

Oxford University Press (OUP)

Subject

Psychiatry and Mental health

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