To investigate the mechanisms underlying
motor hyperactivity, we performed intracisternal
injection of 6‐hydroxydopamine or
endocrine disruptors in rats on postnatal day 5.
6‐Hydroxydopamine (100 μg, 488 nmol) caused
a significant increase in spontaneous motor
activities at 4 weeks of age. Gene‐expression
profiling using a cDNA membrane array
revealed alterations in several classes of gene at
8 weeks of age. In the midbrain, gene expression
was enhanced in dopamine transporter 1; a
platelet‐derived growth factor receptor;
dopamine receptor D4; galanin receptor 2;
arginine vasopressin receptor 2; neuropeptide Y;
tachykinin 2; and fibroblast growth factor 10.
Expression was also enhanced in the
glutamate/aspartate transporter gene in the
striatum. Rats received an endocrine disruptor
(87 nmol), such as bisphenol A, nonylphenol, p‐octylphenol,
or diethylhexylphthalate, which
also caused motor hyperactivity at 4 weeks.
The effects of bisphenol A on motor activity
were dose‐dependent from 0.87 to 87 nmol. The
phenols caused a deficit in dopamine neurons,
similarly to the deficit caused by 6‐hydroxydopamine.
Gene‐expression profiles after
treatment with endocrine disruptors showed
variation and differed from those of 6‐
hydroxydopamine. The results suggest that
neonatal treatment with environmental
chemicals can generate an animal model of
attention‐deficit hyperactivity disorder, in
which clinical symptoms are pervasive.