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Bisphenol A causes hyperactivity in the rat concomitantly with impairment of tyrosine hydroxylase immunoreactivity
Author(s) -
Ishido Masami,
Masuo Yoshinori,
Kunimoto Manabu,
Oka Syuichi,
Morita Masatoshi
Publication year - 2004
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20050
Subject(s) - endocrinology , tyrosine hydroxylase , dopaminergic , medicine , dopamine , dopamine transporter , bisphenol , endocrine disruptor , bisphenol a , biology , chemistry , endocrine system , hormone , organic chemistry , epoxy
We examined the effects of bisphenol A, an endocrine disruptor, on rat behavioral and cellular responses. Single intracisternal administration of bisphenol A (0.2‐20 μg) into 5‐day‐old male Wistar rats caused significant hyperactivity at 4–5 weeks of age. Rats were about 1.6‐fold more active in the nocturnal phase after administration of both 2 and 20 μg of bisphenol A than were control rats. The response was dose‐dependent. Based on DNA macroarray analyses of the midbrain, bisphenol A decreased by more than twofold gene expression levels of the dopamine D4 receptor at 4 weeks of age and the dopamine transporter at 8 weeks of age. Furthermore, bisphenol A decreased by more than twofold gene expression levels of the dopamine D4 receptor at 4 weeks of age and the dopamine transporter at 8 weeks of age. We conclude that bisphenol A affected central dopaminergic system activity, resulting in hyperactivity due most likely to a large reduction of tyrosine hydroxylase activity in the midbrain. © 2004 Wiley‐Liss, Inc.