Abstract
BackgroundWhile striatal dopamine in psychosis and stress has been well studied, the role of dopamine in the prefrontal cortex (PFC) is poorly understood. To date no study has investigated the PFC dopamine response to stress exclusively in schizophrenia or its putative prodrome, even though medial PFC is known as a key area in stress regulation. The present study uses the high-affinity dopamine D2/3 receptor radiotracer [11C]FLB457 and positron emission tomography (PET) together with a validated psychosocial stress challenge to investigate if the PFC dopamine response to stress is dysregulated in schizophrenia and clinical high risk (CHR) for psychosis.MethodsFourteen antipsychotic-free patients with schizophrenia, 14 CHR and 12 matched healthy volunteers underwent two [11C]FLB457 PET scans, one while performing a Sensory Motor Control Task (control) and another while performing the Montreal Imaging Stress Task (stress). PET data were analyzed using the Simplified Reference Tissue Model with non-displaceable binding potential (BPND) as outcome measure. Dopamine release was defined as percent change in BPND between control and stress scan (ΔBPND).ResultsWe observed an increased dopamine release, indexed by ΔBPND, in the medial PFC in schizophrenia patients but not CHR compared to healthy volunteers. Further, associations between stress-induced dopamine release and increase in cortisol levels observed in healthy volunteers and CHR, were absent in schizophrenia, similar to associations with symptoms, distress and anxiety.DiscussionThese findings provide first direct evidence of a disrupted cortical dopamine-stress regulation in schizophrenia.
Highlights
While striatal dopamine in psychosis and stress has been well studied, the role of dopamine in the prefrontal cortex (PFC) is poorly understood
The present study uses the high-affinity dopamine D2/3 receptor radiotracer [11C]FLB457 and positron emission tomography (PET) together with a validated psychosocial stress challenge to investigate if the PFC dopamine response to stress is dysregulated in schizophrenia and clinical high risk (CHR) for psychosis
We observed an increased dopamine release, indexed by ΔBPND, in the medial PFC in schizophrenia patients but not CHR compared to healthy volunteers
Summary
S43 slowing and the cluster showing dyskinesia and abnormal NSS have different cortical-striatal connectivity compared to UHR who show average motor behavior and healthy controls. Discussion: These results provide evidence for etiological theories highlighting altered cortico-striatal networks and the importance of examining motor behavior prior to the onset of psychosis. Taken together, this approach may reflect a novel strategy for promoting tailored risk assessment as well as future research developing individualized medicine. 26.2 CORTICAL STRESS REGULATION IS DISRUPTED IN SCHIZOPHRENIA BUT NOT IN CLINICAL HIGH-RISK FOR PSYCHOSIS. Romina Mizrahi*,1, Alan Wilson, Sylvain Houle, Christin Schifani2 1University of Toronto & Centre for Addiction and Mental Health; 2PET Centre, Centre for Addiction and Mental Health; 3University of Toronto
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