Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin transactivates aryl hydrocarbon receptor-responsive element III in the tyrosine hydroxylase immunoreactive neurons of the mouse midbrain

ABSTRACT Fetal exposure to dioxins and related compounds is known to disrupt normal development of the midbrain dopaminergic system, which regulates behavior, cognition and emotion. The toxicity of these chemicals is mediated mainly by aryl hydrocarbon receptor (AhR) signaling. Previously, we identi...

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Veröffentlicht in:	Journal of applied toxicology 2014-02, Vol.34 (2), p.117-126
Hauptverfasser:	Tanida, Takashi, Tasaka, Ken, Akahoshi, Eiichi, Ishihara-Sugano, Mitsuko, Saito, Michiko, Kawata, Shigehisa, Danjo, Megumi, Tokumoto, Junko, Mantani, Youhei, Nagahara, Daichi, Tabuchi, Yoshiaki, Yokoyama, Toshifumi, Kitagawa, Hiroshi, Kawata, Mitsuhiro, Hoshi, Nobuhiko
Format:	Artikel
Sprache:	eng
Schlagworte:	2,3,7,8‐tetrachlorodibenzo‐p‐dioxin 8-tetrachlorodibenzo-p-dioxin Animals Aromatic compounds aryl hydrocarbon receptor aryl hydrocarbon receptor responsive element III Biocompatibility Brain Dopamine Dopaminergic Neurons - drug effects Dopaminergic Neurons - metabolism Female Fetus - drug effects Fetus - metabolism Genes Hydrocarbons immunohistochemistry Mesencephalon - drug effects Mesencephalon - metabolism Mice Mice, Inbred C57BL Mice, Inbred ICR Mice, Transgenic Neurons Organ Size Pathways Polychlorinated Dibenzodioxins - administration & dosage Polychlorinated Dibenzodioxins - toxicity Pregnancy Prenatal Exposure Delayed Effects Promoter Regions, Genetic Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Rodents Signal Transduction Toxicology Transcriptional Activation Transgenic Tyrosine Tyrosine 3-Monooxygenase - genetics Tyrosine 3-Monooxygenase - metabolism tyrosine hydroxylase
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