Attention deficit hyperactivity disorder (ADHD) is a heritable neurodevelopmental disorder with a reported male predominance that persists into adulthood and leads to significant morbidity in affected individuals. ADHD is currently hypothesized to reflect central dopaminergic dysfunction. Evaluation of human dopaminergic dysfunction using in vivo neuroimaging has been limited to studies of receptor localization and quantification, and dopamine synthesis, rather than direct measurement of the functional status of receptor signaling. There exists a need to thoroughly elucidate mechanisms underlying aberrant dopaminergic neurotransmission downstream of receptor activation in signaling processes. We have developed an in vivo method to measure neuroreceptor-initiated signal transduction involving activation of phospholipase A(2) to release the second messenger, arachidonic acid (AA). We propose to use positron emission tomography (PET) to quantitatively image dopamine-initiated signal transduction via AA in ADHD patients and healthy volunteers, in subjects administered the dopaminergic agonist, apomorphine, and to measure regional cerebral blood flow (rCBF) as well. We hypothesize that signaling and flow responses to apomorphine will be elevated, demonstrating hypersensitivity of the dopamine signaling mechanism.