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Impact of the glucocorticoid receptor BclI polymorphism on reward expectancy and prediction error related ventral striatal reactivity in depressed and healthy individuals

Authors
Ham, Byung-JooGreenberg, TsafrirChase, Henry W.Phillips, Mary L.
Issue Date
1월-2016
Publisher
SAGE PUBLICATIONS LTD
Keywords
Depression; reward; striatum; glucocorticoid; polymorphism; fMRI
Citation
JOURNAL OF PSYCHOPHARMACOLOGY, v.30, no.1, pp.48 - 55
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF PSYCHOPHARMACOLOGY
Volume
30
Number
1
Start Page
48
End Page
55
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/90061
DOI
10.1177/0269881115602486
ISSN
0269-8811
Abstract
There is evidence that reward-related neural reactivity is altered in depressive disorders. Glucocorticoids influence dopaminergic transmission, which is widely implicated in reward processing. However, no studies have examined the effect of glucocorticoid receptor gene polymorphisms on reward-related neural reactivity in depressed or healthy individuals. Fifty-nine depressed individuals with major depressive disorder (n=33) or bipolar disorder (n=26), and 32 healthy individuals were genotyped for the glucocorticoid receptor BclI G/C polymorphism, and underwent functional magnetic resonance imaging during a monetary reward task. We examined the effect of the glucocorticoid receptor BclI G/C polymorphism on reward expectancy (RE; expected outcome value) and prediction error (PE; discrepancy between expected and actual outcome) related ventral striatal reactivity. There was a significant interaction between reward condition and BclI genotype (p=0.007). C-allele carriers showed higher PE than RE-related right ventral striatal reactivity (p<0.001), whereas no such difference was observed in G/G homozygotes. Accordingly, C-allele carriers showed a greater difference between PE and RE-related right ventral striatal reactivity than G/G homozygotes (p<0.005), and also showed lower RE-related right ventral striatal reactivity than G/G homozygotes (p=0.011). These findings suggest a slowed transfer from PE to RE-related ventral striatal responses during reinforcement learning in C-allele carriers, regardless of diagnosis, possibly due to altered dopamine release associated with increased sensitivity to glucocorticoids.
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