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× {{flash.message}} Toggle navigation Toggle navigation 日本語 | English 新規登録ログイン 細川 まゆ子 ホソカワ マユコ  (Mayuko Hosokawa) 更新日: 01/31 ホーム研究キーワード研究分野学歴論文MISC書籍等出版物講演・口頭発表等担当経験のある科目(授業)所属学協会Works(作品等)共同研究・競争的資金等の研究課題 論文 査読有り 2015年11月 Developmental origin of abnormal dendritic growth in the mouse brain induced by in utero disruption of aryl hydrocarbon receptor signaling NEUROTOXICOLOGY AND TERATOLOGY Eiki Kimura Ken-ichiro Kubo Chieri Matsuyoshi Seico Benner Mayuko Hosokawa Toshihiro Endo Wenting Ling Masanobu Kohda Kazuhito Yokoyama Kazunori Nakajima Masaki Kakeyama Chiharu Tohyama … 全て表示 折りたたむ 巻 52 号 Pt A 開始ページ 42 終了ページ 50 記述言語 英語 掲載種別 研究論文（学術雑誌） DOI 10.1016/j.ntt.2015.10.005 出版者・発行元 PERGAMON-ELSEVIER SCIENCE LTD Increased prevalence of mental disorders cannot be solely attributed to genetic factors and is considered at least partly attributable to chemical exposure. Among various environmental chemicals, in utero and lactational dioxin exposure has been extensively studied and is known to induce higher brain function abnormalities in both humans and laboratory animals. However, how the perinatal dioxin exposure affects neuromorphological alterations has remained largely unknown. Therefore, in this study, we initially studied whether and how the overexpression of aryl hydrocarbon receptor (AhR), a dioxin receptor, would affect the dendritic growth in the hippocampus of the developing brain. Transfecting a constitutively active AhR plasmid into the hippocampus via in utero electroporation on gestational day (GD) 14 induced abnormal dendritic branch growth. Further, we observed that 14-day-old mice born to dams administered with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dose: 0, 0.6, or 3.0 mu g/kg) on GD 125 exhibited disrupted dendritic branch growth in both the hippocampus and amygdala. Finally, we observed that 16-month-old mice born to dams exposed to perinatal TCDD as described above exhibited significantly reduced spine densities. These results indicated that abnormal micromorphology observed in the developing brain may persist until adulthood and may induce abnormal higher brain function later in life. (C) 2015 The Authors. Published by Elsevier Inc. リンク情報 DOIhttps://doi.org/10.1016/j.ntt.2015.10.005PubMedhttps://www.ncbi.nlm.nih.gov/pubmed/26526904Web of Sciencehttps://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000367108300006&DestApp=WOS_CPL ID情報 DOI : 10.1016/j.ntt.2015.10.005ISSN : 0892-0362eISSN : 1872-9738PubMed ID : 26526904Web of Science ID : WOS:000367108300006 エクスポート BibTeX RIS 論文リストへ メニュー マイポータル 研究ブログ資料公開 共著者の一覧 まだ共著者が1人も登録されていません。 {{coauthor.Related.name_str}} {{coauthor.Related.last_modified}} 更新 limit"> もっとみる 2017 researchmap 利用規約