No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder

D Hernaus, D Collip, Z Kasanova, O Winz, A Heinzel, T van Amelsvoort, S M Shali, J Booij, Y Rong, M Piel, J Pruessner, F M Mottaghy, I Myin-Germeys

Research output: Contribution to journalArticleAcademicpeer-review

2 Citations (Scopus)

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 [(18)F]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 [(18)F]fallypride displacement and the spatial extent of stress-induced [(18)F]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 [(18)F]fallypride displacement nor the spatial extent of stress-induced [(18)F]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.

Original languageEnglish
Article numbere547
JournalTranslational Psychiatry
Volume5
DOIs
Publication statusPublished - 14 Apr 2015

Keywords

  • Adult
  • Benzamides
  • Brain
  • Case-Control Studies
  • Dopamine
  • Female
  • Fluorine Radioisotopes
  • Humans
  • Male
  • Middle Aged
  • Neostriatum
  • Positron-Emission Tomography
  • Prefrontal Cortex
  • Psychotic Disorders
  • Stress, Psychological
  • Synaptic Transmission
  • Temporal Lobe

Cite this

Hernaus, D ; Collip, D ; Kasanova, Z ; Winz, O ; Heinzel, A ; van Amelsvoort, T ; Shali, S M ; Booij, J ; Rong, Y ; Piel, M ; Pruessner, J ; Mottaghy, F M ; Myin-Germeys, I. / No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder. In: Translational Psychiatry. 2015 ; Vol. 5.
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title = "No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder",
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 [(18)F]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 [(18)F]fallypride displacement and the spatial extent of stress-induced [(18)F]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 [(18)F]fallypride displacement nor the spatial extent of stress-induced [(18)F]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.",
keywords = "Adult, Benzamides, Brain, Case-Control Studies, Dopamine, Female, Fluorine Radioisotopes, Humans, Male, Middle Aged, Neostriatum, Positron-Emission Tomography, Prefrontal Cortex, Psychotic Disorders, Stress, Psychological, Synaptic Transmission, Temporal Lobe",
author = "D Hernaus and D Collip and Z Kasanova and O Winz and A Heinzel and {van Amelsvoort}, T and Shali, {S M} and J Booij and Y Rong and M Piel and J Pruessner and Mottaghy, {F M} and I Myin-Germeys",
year = "2015",
month = "4",
day = "14",
doi = "10.1038/tp.2015.37",
language = "English",
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Hernaus, D, Collip, D, Kasanova, Z, Winz, O, Heinzel, A, van Amelsvoort, T, Shali, SM, Booij, J, Rong, Y, Piel, M, Pruessner, J, Mottaghy, FM & Myin-Germeys, I 2015, 'No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder', Translational Psychiatry, vol. 5, e547. https://doi.org/10.1038/tp.2015.37

No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder. / Hernaus, D; Collip, D; Kasanova, Z; Winz, O; Heinzel, A; van Amelsvoort, T; Shali, S M; Booij, J; Rong, Y; Piel, M; Pruessner, J; Mottaghy, F M; Myin-Germeys, I.

In: Translational Psychiatry, Vol. 5, e547, 14.04.2015.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - No evidence for attenuated stress-induced extrastriatal dopamine signaling in psychotic disorder

AU - Hernaus, D

AU - Collip, D

AU - Kasanova, Z

AU - Winz, O

AU - Heinzel, A

AU - van Amelsvoort, T

AU - Shali, S M

AU - Booij, J

AU - Rong, Y

AU - Piel, M

AU - Pruessner, J

AU - Mottaghy, F M

AU - Myin-Germeys, I

PY - 2015/4/14

Y1 - 2015/4/14

N2 - 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 [(18)F]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 [(18)F]fallypride displacement and the spatial extent of stress-induced [(18)F]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 [(18)F]fallypride displacement nor the spatial extent of stress-induced [(18)F]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.

AB - 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 [(18)F]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 [(18)F]fallypride displacement and the spatial extent of stress-induced [(18)F]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 [(18)F]fallypride displacement nor the spatial extent of stress-induced [(18)F]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.

KW - Adult

KW - Benzamides

KW - Brain

KW - Case-Control Studies

KW - Dopamine

KW - Female

KW - Fluorine Radioisotopes

KW - Humans

KW - Male

KW - Middle Aged

KW - Neostriatum

KW - Positron-Emission Tomography

KW - Prefrontal Cortex

KW - Psychotic Disorders

KW - Stress, Psychological

KW - Synaptic Transmission

KW - Temporal Lobe

U2 - 10.1038/tp.2015.37

DO - 10.1038/tp.2015.37

M3 - Article

C2 - 25871972

VL - 5

JO - Translational Psychiatry

JF - Translational Psychiatry

SN - 2158-3188

M1 - e547

ER -