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Abstract
More than three decades of research has attempted to elucidate the neuropsychopharmacology
of attention-deficit/hyperactivity disorder (ADHD). Stimulants, a principle treatment
for the disorder, act on the norepinephrine (NE) and dopamine (DA) systems; this has
led to a long-standing hypothesis of catecholamine dysfunction in ADHD. Animal studies
show a clear role for NE and DA in the modulation of executive functions, which are
often disturbed in persons with ADHD. Nonstimulant agents that are effective in the
treatment of ADHD tend to affect the NE system, whereas those affecting only DA, or
those that affect neither catecholamine, are less potent in reducing ADHD symptoms.
Studies of the effects of NE and DA peripheral metabolites by ADHD pharmacotherapies
show acute increases in levels of these catecholamines; however, their long-term turnover
may be reduced. Imaging studies suggest stimulants increases DA levels in the brain,
whereas some animal models of ADHD are more consistent with excessive DA activation
in the disorder. Ultimately, ADHD therapy may modify activity in the NE and DA systems
to a more optimal level, thus improving responses to environmental stimuli and enhancing
working memory and executive function.