It has been suggested that impulsive behavior is caused by dysfunctional 
serotonergic 5-HT neurotransmission in the central nervous system (CNS). Brain 
neuroimaging studies have shown that behavioral inhibition is linked to the 
activation of cortex sites such as the ventral frontal cortex. Positron emission 
tomography (PET) imaging with [(18)F]altanserin to characterize 5-HT(2A) 
receptor binding revealed a reduction in 5-HT(2A) binding in the ventral frontal 
cortex in women who had recovered from impulsive diseases. These clinical, 
neuroimaging, and pharmacological studies appear to support the hypothesis that 
functional alteration of neurotransmission due to genetic polymorphisms of the 
5-HT receptors may be involved in impulsive behavior modulation. Following 
evaluation by a self-reporting measure, it was proposed that a polymorphism in 
the promoter of the 5-HT(2A) receptor gene is the underlying cause of impulsive 
behavior; however, this hypothesis is not convincing. We examined whether the 
polymorphism in the 5-HT(2A) receptor gene promoter is involved in impulsive 
aggression by evaluating a behavioral task (Go/No-go task) in normal volunteers. 
The polymorphism of the 5-HT(2A) receptor gene promoter in lymphocytes from 71 
volunteers was analyzed by using PCR. Impulsivity was defined as the number of 
commission errors (responding when one should not) recorded during a Go/No-go 
task; a larger number of commission errors indicate greater difficulty in 
inhibiting impulsive behavior. The subjects of the A-1438A allele group for the 
5-HT(2A) receptor gene made more commission errors under the punishment-reward 
(PR)condition in a Go/No-go task than those in the G-1438G group. In the present 
review, we discuss and suggest the possible involvement of the A-1438A 
polymorphism of the 5HT2A receptor gene promoter in impulsive behavior. This 
hypothesis was evaluated by using a behavioral task measure that could directly 
reveal impulsive behavioral traits in humans.