Electrophysiological markers of attention deficit—hyperactivity disorder (ADHD) imply a deficit in frontoparietal function, evidenced by alterations in the P300 wave associated with oddball-type tasks. There are also differences between ADHD and control subjects in potentials related to monitoring and detection of errors, such as the frontomedial negativity, which has been attributed to activation of the ventromedial prefrontal cortex and anterior cingulate cortex. Finally, quantitative electroencephalography (measuring absolute spectral power and frequency distribution) has reappeared in the last few years with consistent findings that would permit the discrimination of clinical subtypes. Genetic studies of ADHD have been oriented to linkage analysis in affected families and to the study of candidate genes. Most of these genes codify proteins related to neurotransmitter transmission, specifically dopaminergic, serotoninergic, and noradrenergic. In accordance with the neurobio-logical basis for ADHD, consisting of a relative prefrontal dysfunction, those genes showing a more consistent association with this condition relate to dopaminergic transmission, a selective regulator of frontal lobe dynamics. An example of this is the dopamine receptor DRD4, but there are other genes which will be reviewed in this chapter. The combination of genetic and electrophysiological analyses promises to be an excellent approach to the neurobiological bases of diverse neuropsychiatric disorders, among them ADHD.