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Cited by 118Neurotransmitter Receptor Influence on BehaviorNeural and Behavioral Psychology StudiesSchizophrenia research and treatment

The DOI matches its Crossref record; 71 of the 72 references it cites were found in a registry or an index.

Genetic markers of striatal dopamine predict individual differences in dysfunctional, but not functional impulsivity

Colzato, L.S., van den Wildenberg, W.P.M., Van der Does, A.J.W., Hommel, B.·2010·Neuroscience
DOI 10.1016/j.neuroscience.2010.07.050
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Abstract

Various psychiatric disorders are characterized by elevated levels of impulsivity. Although extensive evidence supports a specific role of striatal, but not frontal dopamine (DA) in human impulsivity, recent studies on genetic variability have raised some doubts on such a role. Importantly, impulsivity consists of two dissociable components that previous studies have failed to separate: functional and dysfunctional impulsivity. We compared participants with a genetic predisposition to have relatively high striatal DA levels (DAT1 9-repeat carriers, DRD2 C957T T/T homozygotes, and DRD4 7-repeat carriers) with participants with other genetic predispositions. We predicted that the first group would show high scores of dysfunctional, but not functional, self-reported impulsivity and greater difficulty in inhibiting a behavioral response to a stop-signal, a behavioral measure of impulsivity. In a sample of 130 healthy adults, we studied the relation between DAT1, DRD4, and C957T polymorphism at the DRD2 gene (polymorphisms related to striatal DA) and catechol-Omethyltransferase (COMT) Val158Met (a polymorphism related to frontal DA) on self-reported dysfunctional and functional impulsivity, assessed by the Dickman impulsivity inventory (DII), and the efficiency of inhibitory control, assessed by the stop-signal paradigm. DRD2 C957T T/T homozygotes and DRD4 7-repeat carriers indeed had significantly higher scores on self-reported dysfunctional, but not functional, impulsivity. T/T homozygotes were also less efficient in inhibiting prepotent responses. Our findings support the claim that dopaminergic variation affects dysfunctional impulsivity. This is in line with the notion that the over-supply of striatal DA might weaken inhibitory pathways, thereby enhancing the activation of, and the competition between responses.

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Metadata

Authors
Colzato, L. S., van den Wildenberg, W. P. M., Van der Does, A. J. W., & Hommel, B.
Affiliations
Leiden University (NL)
Corresponding author
Colzato, L.S.
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2010-10
Volume
170
Issue
3
Pages
782-788
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2010.07.050
OpenAlex
W2143738475
Cited by
117
References
72
Citations by year
2025: 2 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 7 · 2019: 2 · 2018: 7 · 2017: 10 · 2016: 11 · 2015: 12 · 2014: 20 · 2013: 8 · 2012: 12
FWCI
4.12
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • UvA-DARE (University of Amsterdam) (publishedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Leiden Repository (Leiden University) (submittedVersion)
  • UvA-DARE (University of Amsterdam) (submittedVersion)
Funders
Netherlands Organization for Scientific Research
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Keywords
dysfunctional impulsivity, functional impulsivity, striatal dopamine, COMT Val158Met polymorphism, inhibitory control, stop-signal task, genetic susceptibility, individual differences, response inhibition
MeSH terms
Adult, Catechol O-Methyltransferase, Corpus Striatum, Dopamine, Female, Genetic Markers, Humans, Impulsive Behavior, Inhibition, Psychological, Intelligence, Male, Polymorphism, Genetic, Receptors, Dopamine D2, Genetic Predisposition to Disease, Dopamine Plasma Membrane Transport Proteins, Receptors, Dopamine D4, Self Report

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