Abstract
Cocaine addiction involves a number of medical, psychological and social problems. Understanding the genetic aetiology of this disorder will be essential for design of effective treatments. Dopamine-beta hydroxylase (DbH) catalyzes the conversion of dopamine to norepinephrine and could, therefore, have an influence on both cocaine action and the basal sensitivity of neurotransmitter systems to cocaine. Recently, the -1021C>T polymorphism have been found to strongly correlated with individual variation in plasma DbH activity. To test the influence of this polymorphism on the susceptibility of cocaine addiction, we decided to genotype it in a sample of 689 cocaine addicts and 832 healthy individuals. Genotypic and allelic analyses did not show any evidence of association with cocaine addiction, even after correcting for the effect of population stratification and other possible confounders. Our results do not support a major role of the -1021C>T polymorphism or the gene itself in the development of cocaine addiction but further examination of other variants within this gene will be necessary to completely rule out an effect.
Highlights
Cocaine's potent actions in blocking the uptake by neuronal plasma membrane transporters for dopamine (DAT), serotonin (SERT), and norepinephrine (NET) are well known [4]
Twin and family studies have demonstrated that cocaine addiction has a strong genetic component but the exact basis of the heritable factors that have a significant contribution to this phenotype remain unclear [3]
Using extreme phenotypes in samples from African and European American and Japanese populations, Zabetian and co-workers [16] reported that the 1021C>T polymorphism located in the 5' flanking region of the gene accounted for between 35– 52% of the variation in plasma Dopaminebeta hydroxylase (DbH) activity in these populations
Summary
Cocaine's potent actions in blocking the uptake by neuronal plasma membrane transporters for dopamine (DAT), serotonin (SERT), and norepinephrine (NET) are well known [4]. Using extreme phenotypes in samples from African and European American and Japanese populations, Zabetian and co-workers [16] reported that the 1021C>T polymorphism (rs1611115) located in the 5' flanking region of the gene accounted for between 35– 52% of the variation in plasma DbH activity in these populations.
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