Variation in dopamine genes influences responsivity of the human reward system
Open accessAbstract
In humans, dopamine neurotransmission is influenced by functional polymorphisms in the dopamine transporter (DAT1) and catechol-O-methyltransferase (COMT) genes. Here, we used event-related functional magnetic resonance imaging to directly investigate the neurofunctional effects of the Val(158)Met COMT and variable number of tandem repeat DAT1 polymorphisms on distinct components of the reward system in humans. The results revealed a main effect of COMT genotype in the ventral striatum and lateral prefrontal cortex during reward anticipation (P < 0.001, uncorrected) and in the orbitofrontal cortex at the time of reward delivery (P < 0.005), met/met individuals exhibiting the highest activation. The main effect of DAT1 genotype was seen in robust blood-oxygen-level-dependent response differences in the caudate nucleus and ventral striatum during reward anticipation (P < 0.001) and in the lateral prefrontal cortex and midbrain at the time of reward delivery, with carriers of the DAT1 9-repeat allele showing the highest activity. Moreover, an interaction between the COMT and DAT1 genes was found in the ventral striatum and lateral prefrontal cortex during reward anticipation and in the lateral prefrontal and orbitofrontal cortices as well as in the midbrain at the time of reward delivery, with carriers of the DAT1 9-repeat allele and COMT met/met allele exhibiting the highest activation, presumably reflecting functional change consequent to higher synaptic dopamine availability. Taken together, these results indicate that genetically influenced variations in dopamine transmission modulate the response of brain regions involved in anticipation and reception of rewards and suggest that these responses may contribute to individual differences in reward-seeking behavior and in predisposition to neuropsychiatric disorders.
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Valid endophenotypes can be found at a higher rate in unaffected family members than in the general population.
“it has been proposed that valid endophenotypes can be found at a higher rate in unaffected family members than in the general population 23,24.”
From Increased neural responses to reward in adolescents and young adults with attention-deficit/hyperactivity disorder and their unaffected siblings (2015) · cites this paper as [23]
The Results and Conclusion (pages not provided) discuss dopamine genotypes and reward-related brain activity, not the prevalence of endophenotypes among unaffected family members. Searches for endophenotypes and unaffected relatives found no passage comparing them with the general population. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe function of the reward circuitry can be modulated by functional genetic polymorphisms influencing dopamine neurotransmission in the striatum, directly (e.g. DAT1) or indirectly (e.g. NOS1).
“The function of the reward circuitry can be modulated by functional genetic polymorphisms influencing dopamine neurotransmission in the striatum, directly (e.g. the dopamine transporter gene [DAT1]) or indirectly (e.g. the nitric oxide synthase gene [NOS1]).18,22,26”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [26]
The caudate nucleus is a core region of the dopamine reward-circuit, implicated in ADHD-control differences, and genetic variation in DAT1 is reported to affect its function and structure.
“The caudate nucleus is a core region of the dopamine reward-circuit,42 implicated in ADHD-control differences,4 and genetic variation in DAT1 is reported to affect its function and structure 26,43”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [26]
This finding confirms previous evidence that genetic variation in DAT1 modulates striatal reward-related activation.
“This finding confirms previous evidence from healthy volunteers that genetic variation in DAT1 modulates striatal reward-related activation.26,49,50”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [26]
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- Authors
- Dreher, J.-C., Kohn, P., Kolachana, B., Weinberger, D. R., & Berman, K. F.
- Affiliations
- Section on Integrative Neuroimaging,
- National Institutes of Health (US)
- Corresponding author
- Dreher, Jean-Claude
- Berman, Karen Faith
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-01-13
- Volume
- 106
- Issue
- 2
- Pages
- 617-622
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2626752
- OpenAlex
- W2108092648
- Cited by
- 376
- References
- 44
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- FWCI
- 11.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- 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
- dopamine, reward systems, dopamine transporter gene, COMT Val158Met polymorphism, variable number tandem repeats, reward anticipation, reward processing, ventral striatum, orbitofrontal cortex, lateral prefrontal cortex, caudate nucleus, midbrain, gene-gene interaction, individual differences, reward-seeking behavior, neuropsychiatric disorders
- MeSH terms
- Basal Ganglia, Brain Mapping, Catechol O-Methyltransferase, Dopamine, Genotype, Humans, Magnetic Resonance Imaging, Mesencephalon, Synaptic Transmission, Oxygen, Polymorphism, Genetic, Reward, Prefrontal Cortex, Minisatellite Repeats, Mutation, Missense, Dopamine Plasma Membrane Transport Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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