Abstract:
OBJECTIVE:The sensitivity of dopamine reward pathways has been implicated in the risk for various psychiatric disorders including compulsive overeating. The evidence is divided, however, about the direction of causal association. One argument is that a Reward Deficiency Syndrome is the risk factor, while others contend that hyper-sensitivity to reward enhances the motivation for pleasurable activities like eating. Unfortunately, little human research has bridged the gap between psychological and neurobiological approaches to brain reward functioning and disorder. The present study addressed this issue by implementing psychological and biological markers of reward sensitivity in the assessment protocol. METHODS:Adults with binge eating disorder (BED) were compared to samples of normal-weight and obese controls on two personality measures of reward sensitivity and were genotyped for six markers of the DRD2 dopamine receptor gene. RESULTS:Genotype x Group ANOVAs revealed significant main effects and an interaction on the personality measures for Taq1A. BED and obese subjects reported greater reward sensitivity than normal-weight controls, but only among those carrying the A1 allele. We also found that normal-weight controls with at least one copy of the T allele of the C957T marker had significantly lower reward sensitivity scores than any of the other groups who did not differ from each other. CONCLUSIONS:Given evidence linking the A1 allele with reduced receptor density, an inverse relationship was expected between psychological measures of reward sensitivity and presence of the A1 allele. One explanation for our findings could be that the BED and obese participants possess another genetic variant that interacts with the A1 allele to produce higher dopamine activity. These findings have implications for future studies of the molecular genetics of BED and obesity, and for behavioural and pharmacologic therapies targeting these conditions.
journal_name
Prog Neuropsychopharmacol Biol Psychiatryauthors
Davis C,Levitan RD,Kaplan AS,Carter J,Reid C,Curtis C,Patte K,Hwang R,Kennedy JLdoi
10.1016/j.pnpbp.2007.09.024subject
Has Abstractpub_date
2008-04-01 00:00:00pages
620-8issue
3eissn
0278-5846issn
1878-4216pii
S0278-5846(07)00349-1journal_volume
32pub_type
杂志文章abstract::1. Studies on the metabolism of the tricyclic antidepressant trimipramine (TMP) in the rat are described. 2. Twenty metabolites of TMP were isolated from rat urine after enzymatic hydrolysis and their structures were determined by a gas chromatographic-mass spectrometric (GC-MS) method. 3. Twelve TMP metabolites were ...
journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.pnpbp.2007.04.014
更新日期:2007-08-15 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
pub_type: 杂志文章
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更新日期:1995-05-01 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
pub_type: 杂志文章,评审
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更新日期:1985-01-01 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
pub_type: 杂志文章,评审
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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pub_type: 杂志文章
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