Attention-deficit/hyperactivity disorder (ADHD) is a primarily pediatric condition with hallmark behavioral signs of inattention, impulsivity, and hyperactivity that often lead to poor performance in both academic endeavors and social function. Given the heterogenous nature of this disorder, animal studies on the etiology of ADHD have taken several approaches including selective breeding, genetic deletion, perinatal insult, and neonatal lesion. A classic approach is use of spontaneously hypertensive rats, which display elevated inattention, impulsivity, and hyperactivity and show disruptions in dopamine neurotransmission. The lateral habenula regulates dopamine transmission to the forebrain and disruption of this circuit in rodents produces these same behavioral impairments . This raises the possibility that impairment of this circuit is an as yet unstudied mechanism by which ADHD-like behaviors manifest. We are currently using SHR rats to test the hypothesis that an impaired habenulo-mesencephalic circuit significantly contributes to ADHD-like behavior.