INTRODUCTION Previous research has suggested brain dopamine (DA) neurotransmission to be involved in the control of ejaculation. Furthermore, previous studies indicate a partly hereditary background to premature ejaculation.\nAIM\nTo investigate whether the dopamine transporter gene (DAT1) polymorphism is associated with premature ejaculation. METHODS Retrospective self-reports of four indicators reflecting ejaculatory function-anteportal ejaculation, number of penile thrusts, ejaculation latency time, and feeling of control over ejaculation-and saliva samples for DNA analysis were obtained from 1,290 men (M = 26.9, standard deviation = 4.7 years; range 18-45) with sexual experience. Main Outcome Measures. Calculations of allelic effects were computed using the Generalized Estimating Equations module of SPSS 17. RESULTS Carriers of the 10R10R genotype had scores indicating a lower threshold to ejaculate on each of the indicators compared to the combined 9R9R/9R10R carrier group. The differences were significant both for the composite score and for anteportal ejaculation, number of thrusts, and feeling of control over ejaculation, but not for ejaculation latency time. The effect of the polymorphism remained significant after controlling for age, homosexual experience, having a regular sexual partner, level of sexual desire, and frequency of sexual activity, hence suggesting that it is not secondary to an association between the studied polymorphism and some other aspect of sexual behavior, but due to a specific influence of DA on ejaculation. CONCLUSIONS The findings of the present study support results of previous studies indicating involvement of dopaminergic neurotransmission in ejaculation.