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  1. 0 資料タイプ別
  2. 02 学位論文
  1. 250 大学院医歯学総合研究科(医)
  2. 60 博士学位論文
  3. 10 博士学位論文

Brain hyperserotonemia causes autism-relevant social deficits in mice

http://hdl.handle.net/10191/51320
http://hdl.handle.net/10191/51320
d7ed8472-ac65-47f9-abf5-8d484f79085b
名前 / ファイル ライセンス アクション
h30nmk842.pdf 本文 (3.8 MB)
h30nmk842_a.pdf 要旨 (791.3 kB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2019-07-09
タイトル
タイトル Brain hyperserotonemia causes autism-relevant social deficits in mice
タイトル
言語 en
タイトル Brain hyperserotonemia causes autism-relevant social deficits in mice
言語
言語 eng
資源タイプ
資源 http://purl.org/coar/resource_type/c_46ec
タイプ thesis
その他のタイトル
その他のタイトル 脳のセロトニン過剰はマウスで自閉症関連の社会的障害を引き起こす
著者 Tanaka, Miho

× Tanaka, Miho

WEKO 175129

Tanaka, Miho

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著者別名
識別子 175130
識別子Scheme WEKO
姓名 田中, 美歩
抄録
内容記述タイプ Abstract
内容記述 Background: Hyperserotonemia in the brain is suspected to be an endophenotype of autism spectrum disorder(ASD). Reducing serotonin levels in the brain through modulation of serotonin transporter function may improve ASD symptoms.
Methods: We analyzed behavior and gene expression to unveil the causal mechanism of ASD-relevant social deficits using serotonin transporter (Sert) knockout mice.
Results: Social deficits were observed in both heterozygous knockout mice (HZ) and homozygous knockout mice (KO), but increases in general anxiety were only observed in KO mice. Two weeks of dietary restriction of the serotonin precursor tryptophan ameliorated both brain hyperserotonemia and ASD-relevant social deficits in Sert HZ and KO mice. The expression of rather distinct sets of genes was altered in Sert HZ and KO mice, and a substantial portion of these genes was also affected by tryptophan depletion. Tryptophan depletion in Sert HZ and KO mice was associated with alterations in the expression of genes involved in signal transduction pathways initiated by changes in extracellular serotonin or melatonin, a derivative of serotonin. Only expression of the AU015836 gene was altered in both Sert HZ and KO mice. AU015836 expression and ASD-relevant social deficits normalized after dietary tryptophan restriction.
Conclusions: These findings reveal a Sert gene dose-dependent effect on brain hyperserotonemia and related behavioral sequelae in ASD and a possible therapeutic target to normalize brain hyperserotonemia and ASD-relevant social deficits.
Keywords: Serotonin transporter, Tryptophan depletion, Autism spectrum disorder, Heterozygous mice
内容記述
内容記述タイプ Other
内容記述 学位の種類: 博士(医学). 報告番号: 甲第4520号. 学位記番号: 新大院博(医)甲第842号. 学位授与年月日: 平成31年3月25日
書誌情報 発行日 2019-03-25
出版者
出版者 新潟大学
権利
権利情報 【○!C】The Author(s). 2018
著者版フラグ
値 ETD
学位名
学位名 博士(医学)
学位授与機関
学位授与機関名 新潟大学
学位授与年月日
学位授与年月日 2019-03-25
学位授与番号
学位授与番号 13101甲第4520号
学位記番号
内容記述タイプ Other
内容記述 新大院博(医)甲第842号
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