Striatal dopamine in anhedonia: A simultaneous [
Anhedonia
Dopamine
Mesolimbic
PET-MR
Reward
Self-reported stress
Journal
Psychiatry research. Neuroimaging
ISSN: 1872-7506
Titre abrégé: Psychiatry Res Neuroimaging
Pays: Netherlands
ID NLM: 101723001
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
received:
07
11
2022
revised:
21
04
2023
accepted:
18
05
2023
pmc-release:
01
08
2024
medline:
7
7
2023
pubmed:
11
6
2023
entrez:
10
6
2023
Statut:
ppublish
Résumé
Anhedonia is hypothesized to be associated with blunted mesocorticolimbic dopamine (DA) functioning in samples with major depressive disorder. The purpose of this study was to examine linkages between striatal DA, reward circuitry functioning, anhedonia, and, in an exploratory fashion, self-reported stress, in a transdiagnostic anhedonic sample. Participants with (n = 25) and without (n = 12) clinically impairing anhedonia completed a reward-processing task during simultaneous positron emission tomography and magnetic resonance (PET-MR) imaging with [ Relative to controls, the anhedonia group exhibited decreased task-related DA release in the left putamen, caudate, and nucleus accumbens and right putamen and pallidum. There were no group differences in task-related brain activation (fMRI) during reward processing after correcting for multiple comparisons. General functional connectivity (GFC) findings revealed blunted fMRI connectivity between PET-derived striatal seeds and target regions in the anhedonia group. Associations were identified between anhedonia severity and the magnitude of task-related DA release to rewards in the left putamen, but not mesocorticolimbic GFC. Results provide evidence for reduced striatal DA functioning during reward processing and blunted mesocorticolimbic network functional connectivity in a transdiagnostic sample with clinically significant anhedonia.
Sections du résumé
BACKGROUND
Anhedonia is hypothesized to be associated with blunted mesocorticolimbic dopamine (DA) functioning in samples with major depressive disorder. The purpose of this study was to examine linkages between striatal DA, reward circuitry functioning, anhedonia, and, in an exploratory fashion, self-reported stress, in a transdiagnostic anhedonic sample.
METHODS
Participants with (n = 25) and without (n = 12) clinically impairing anhedonia completed a reward-processing task during simultaneous positron emission tomography and magnetic resonance (PET-MR) imaging with [
RESULTS
Relative to controls, the anhedonia group exhibited decreased task-related DA release in the left putamen, caudate, and nucleus accumbens and right putamen and pallidum. There were no group differences in task-related brain activation (fMRI) during reward processing after correcting for multiple comparisons. General functional connectivity (GFC) findings revealed blunted fMRI connectivity between PET-derived striatal seeds and target regions in the anhedonia group. Associations were identified between anhedonia severity and the magnitude of task-related DA release to rewards in the left putamen, but not mesocorticolimbic GFC.
CONCLUSIONS
Results provide evidence for reduced striatal DA functioning during reward processing and blunted mesocorticolimbic network functional connectivity in a transdiagnostic sample with clinically significant anhedonia.
Identifiants
pubmed: 37301129
pii: S0925-4927(23)00070-7
doi: 10.1016/j.pscychresns.2023.111660
pmc: PMC10594643
mid: NIHMS1909261
pii:
doi:
Substances chimiques
Raclopride
430K3SOZ7G
Dopamine
VTD58H1Z2X
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
111660Subventions
Organisme : NIMH NIH HHS
ID : K23 MH113733
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH111676
Pays : United States
Organisme : NIMH NIH HHS
ID : R21 MH110933
Pays : United States
Organisme : NIMH NIH HHS
ID : R61 MH110027
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH095809
Pays : United States
Organisme : NIMH NIH HHS
ID : R33 MH110027
Pays : United States
Organisme : NIMH NIH HHS
ID : R37 MH068376
Pays : United States
Organisme : NIMH NIH HHS
ID : F31 MH130107
Pays : United States
Informations de copyright
Copyright © 2023 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest Over the past 3 years, Dr. Pizzagalli has received consulting fees from Albright Stonebridge Group, Boehringer Ingelheim, Compass Pathways, Engrail Therapeutics, Neumora Therapeutics (formerly BlackThorn Therapeutics), Neurocrine Biosciences, Neuroscience Software, Otsuka, Sunovion, and Takeda; he has received honoraria from the Psychonomic Society (for editorial work) and from Alkermes; he has received research funding from the Brain and Behavior Research Foundation, the Dana Foundation, Millennium Pharmaceuticals, and NIMH; he has received stock options from Compass Pathways, Engrail Therapeutics, Neumora Therapeutics, and Neuroscience Software. No funding from these entities was used to support the current work, and all views expressed are solely those of the authors. The other authors have no conflicts of interest or relevant disclosures.
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