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Replication study implicates COMT val158met polymorphism as a modulator of probabilistic reward learning

Lancaster, Thomas, Heerey, E. A., Mantripragada, Kiran Kumar and Linden, David Edmund Johannes 2015. Replication study implicates COMT val158met polymorphism as a modulator of probabilistic reward learning. Genes Brain and Behaviour 14 (6) , pp. 486-492. 10.1111/gbb.12228

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Abstract

Previous studies suggest that a single nucleotide polymorphism in the catechol-O-methyltransferase (COMT) gene (val158met) may modulate reward-guided decision making in healthy individuals. The polymorphism affects dopamine catabolism and thus modulates prefrontal dopamine levels, which may lead to variation in individual responses to risk and reward. We previously showed, using tasks that index reward responsiveness (measured by responses bias towards reinforced stimuli) and risk taking (measured by the Balloon Analogue Risk Task), that COMT met homozygotes had increased reward responsiveness and, thus, an increased propensity to seek reward. In this study, we sought to replicate these effects in a larger, independent cohort of Caucasian UK university students and staff with similar demographic characteristics (n = 101; 54 females, mean age: 22.2 years). Similarly to our previous study, we observed a significant trial × COMT genotype interaction (P = 0.047; η2 = 0.052), which was driven by a significant effect of COMT on the incremental acquisition of response bias [response bias at block 3 − block 1 (met/met > val/val: P = 0.028) and block 3 − block 2 (met/met > val/val: P = 0.007)], suggesting that COMT met homozygotes demonstrated higher levels of reward responsiveness by the end of the task. However, we failed to see main effects of COMT genotype on overall response bias or risk-seeking behaviour. These results provide additional evidence that prefrontal dopaminergic variation may have a role in reward responsiveness, but not risk-seeking behaviour. Our findings may have implications for neuropsychiatric disorders characterized by clinical deficits in reward processing such as anhedonia.

Item Type: Article
Date Type: Publication
Status: Published
Schools: MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Medicine
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords: Anhedonia; BART; COMT; dopamine; genetics; prefrontal; reward responsiveness; reward seeking; signal detection; val158met
Publisher: Wiley-Blackwell
Date of Acceptance: 18 June 2015
Last Modified: 25 Dec 2017 20:23
URI: http://orca.cf.ac.uk/id/eprint/81938

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