| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4180835 | Biological Psychiatry | 2006 | 7 Pages |
BackgroundPrevious evidence has shown that genetic variations in the serotonergic system contribute to individual differences in personality traits germane to impulse control. The monoamine oxidase-A (MAO-A) gene, coding for an enzyme primarily involved in serotonin and noradrenaline catabolism, presents a well-characterized functional polymorphism consisting of a variable number of tandem repeats in the promoter region, with high-activity and low-activity variants. High-activity allele carriers have higher enzyme expression, lower amine concentration, and present higher scores on behavioral measures of impulsivity than low-activity allele carriers.MethodsWe studied the relationship of this polymorphism to brain activity elicited by a response inhibition task (Go/NoGo task), using blood oxygenation level–dependent (BOLD) functional magnetic resonance imaging in 24 healthy men.ResultsDirect comparison between groups revealed a greater BOLD response in the right ventrolateral prefrontal cortex (Brodmann’s area [BA] 45/47) in high-activity allele carriers, whereas a greater response in the right superior parietal cortex (BA 7) and bilateral extrastriate cortex (BA 18) was found in low-activity allele carriers.ConclusionsThese data suggest that a specific genetic variation involving serotonergic catabolism can modulate BOLD response associated with human impulsivity.
