There may be common etiological pathways to ADHD and the behavioral phenotype of FASD. Alternatively, acquired ADHD secondary to prenatal alcohol exposure may be due to the effect of alcohol on the developing dopamine transmitter system. These two hypotheses are supported by changes in the neurochemistry seen in animal studies of fetal alcohol exposure in which deficits have been found in most neurotransmitter systems, including the dopaminergic, noradrenergic, serotonergic, cholinergic, glutaminergic, gamma aminobutyric acid (GABA)-ergic, and histaminergic systems. Deficits in noradrenergic and dopaminergic systems are the most likely ones to be related to the ADHD symptoms seen in animals with prenatal alcohol exposure. The D1 receptors of the mesolimbic dopamine system tend to be affected by alcohol exposure more than other dopamine systems.6
