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 (pages 117–126)
Takashi Tanida, Ken Tasaka, Eiichi Akahoshi, Mitsuko Ishihara-Sugano, Michiko Saito, Shigehisa Kawata, Megumi Danjo, Junko Tokumoto, Youhei Mantani, Daichi Nagahara, Yoshiaki Tabuchi, Toshifumi Yokoyama, Hiroshi Kitagawa, Mitsuhiro Kawata and Nobuhiko Hoshi
Article first published online: 8 JAN 2013 | DOI: 10.1002/jat.2839
Previously, we identified the novel binding motif of aryl hydrocarbon receptor (AhR), “AhR-responsive element III (AHRE-III)” upstream from the tyrosine hydroxylase (TH) gene. We investigated whether or not 2,3,7,8”tetrachlorodibenzo-p-dioxin (TCDD) could regulate AHRE-III transcriptional activitywithin TH-immunoreactive (ir) neurons of midbrain dopaminergic nuclei. Using transgenic mice, it was demonstrated that fetal exposure to TCDD significantly increased TH-ir intensity and the numbers of TH-ir neurons within midbrain at 8 wk. It is suggested that this increase is caused via AhR-AHRE-III-mediated pathway.