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Yoshihiro Iwasa - One of the best experts on this subject based on the ideXlab platform.

Kazuhiro Marumoto - One of the best experts on this subject based on the ideXlab platform.

Taishi Takenobu - One of the best experts on this subject based on the ideXlab platform.

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Ye Rong - One of the best experts on this subject based on the ideXlab platform.

  • No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder.
    Translational psychiatry, 2015
    Co-Authors: Dennis Hernaus, Dina Collip, Zuzana Kasanova, Oliver Winz, Alexander Heinzel, T. Van Amelsvoort, Siamak Mohammadkhani Shali, J. Booij, Ye Rong
    Abstract:

    Stress is an important risk factor in the etiology of psychotic disorder. Preclinical work has shown that stress primarily increases dopamine (DA) transmission in the frontal cortex. Given that DA-mediated hypofrontality is hypothesized to be a cardinal feature of psychotic disorder, stress-related extrastriatal DA release may be altered in psychotic disorder. Here we quantified for the first time stress-induced extrastriatal DA release and the Spatial Extent of extrastriatal DA release in individuals with non-affective psychotic disorder (NAPD). Twelve healthy volunteers (HV) and 12 matched drug-free NAPD patients underwent a single infusion [18F]fallypride positron emission tomography scan during which they completed the control and stress condition of the Montreal Imaging Stress Task. HV and NAPD did not differ in stress-induced [18F]fallypride displacement and the Spatial Extent of stress-induced [18F]fallypride displacement in medial prefrontal cortex (mPFC) and temporal cortex (TC). In the whole sample, the Spatial Extent of stress-induced radioligand displacement in right ventro-mPFC, but not dorso-mPFC or TC, was positively associated with task-induced subjective stress. Psychotic symptoms during the scan or negative, positive and general subscales of the Positive and Negative Syndrome Scale were not associated with stress-induced [18F]fallypride displacement nor the Spatial Extent of stress-induced [18F]fallypride displacement in NAPD. Our results do not offer evidence for altered stress-induced extrastriatal DA signaling in NAPD, nor altered functional relevance. The implications of these findings for the role of the DA system in NAPD and stress processing are discussed.