7 research outputs found
Effects of Neonatal Treatment With 6-Hydroxydopamine and Endocrine Disruptors on Motor Activity and Gene Expression in Rats
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