Please use this identifier to cite or link to this item: https://doi.org/10.3389/fnins.2012.00054
Title: Why some people discount more than others: Baseline activation in the dorsal PFC mediates the link between COMT genotype and impatient choice
Authors: Gianotti, L.R.R.
Figner, B.
Ebstein, R.P. 
Knoch, D.
Keywords: COMT genotype
Delay discounting
Endophenotype
Individual differences
Intertemporal choice
Resting EEG
Issue Date: 2012
Source: Gianotti, L.R.R.,Figner, B.,Ebstein, R.P.,Knoch, D. (2012). Why some people discount more than others: Baseline activation in the dorsal PFC mediates the link between COMT genotype and impatient choice. Frontiers in Neuroscience (MAY) : -. ScholarBank@NUS Repository. https://doi.org/10.3389/fnins.2012.00054
Abstract: Individuals differ widely in how steeply they discount future rewards. The sources of these stable individual differences in delay discounting (DD) are largely unknown. One candidate is the COMTVal158Met polymorphism, known to modulate prefrontal dopamine levels and affect DD. To identify possible neural mechanisms by which this polymorphism may contribute to stable individual DD differences, we measured 73 participants' neural baseline activation using resting electroencephalogram (EEG). Such neural baseline activation measures are highly heritable and stable over time, thus an ideal endophenotype candidate to explain how genes may influence behavior via individual differences in neural function. After EEG-recording, participants made a series of incentive-compatible intertemporal choices to determine the steepness of their DD. We found that COMT significantly affected DD and that this effect was mediated by baseline activation level in the left dorsal prefrontal cortex (DPFC): (i) COMT had a significant effect on DD such that the number of Val alleles was positively correlated with steeper DD (higher numbers of Val alleles means greater COMT activity and thus lower dopamine levels). (ii) A whole-brain search identified a cluster in left DPFC where baseline activation was correlated with DD; lower activation was associated with steeper DD. (iii) COMT had a significant effect on the baseline activation level in this left DPFC cluster such that a higher number of Val alleles was associated with lower baseline activation. (iv) The effect of COMT on DD was explained by the mediating effect of neural baseline activation in the left DPFC cluster. Our study thus establishes baseline activation level in left DPFC as salient neural signature in the form of an endophenotype that mediates the link between COMT and DD. © 2012 Gianotti, Figner, Ebstein and Knoch.
Source Title: Frontiers in Neuroscience
URI: http://scholarbank.nus.edu.sg/handle/10635/49891
ISSN: 16624548
DOI: 10.3389/fnins.2012.00054
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