Brain hyperserotonemia causes autism-relevant social deficits in mice

Persistent ID (NDL): info:ndljp/pid/11498340

Material type: 博士論文

Author: Tanaka, Miho

Publisher: 新潟大学

Publication date: 2019-03-25

Material Format: Digital

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Name of awarding university/degree: 新潟大学,博士（医学）

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Note (General)：: Background: Hyperserotonemia in the brain is suspected to be an endophenotype of autism spectrum disorder(ASD). Reducing serotonin levels in the brain...

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Material Type: 博士論文
Title: Brain hyperserotonemia causes autism-relevant social deficits in mice
Author/Editor: Tanaka, Miho
Publication, Distribution, etc.: 新潟大学
Publication Date: 2019-03-25
Publication Date (W3CDTF): 2019-03-25
Alternative Title: Brain hyperserotonemia causes autism-relevant social deficits in mice
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
Degree grantor/type: 新潟大学
Date Granted: 2019-03-25
Date Granted (W3CDTF): 2019-03-25
Dissertation Number: 甲第4520号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第4520号
Text Language Code: eng
Note (General): 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
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
新大院博（医）甲第842号
元資料の権利情報 : 【○!C】The Author(s). 2018
Persistent ID (NDL): info:ndljp/pid/11498340
https://dl.ndl.go.jp/pid/11498340
Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2020-06-07T00:39:19+09:00
Date Created (W3CDTF): 2019-09-10
Format (IMT): application/pdf
Access Restrictions: 国立国会図書館内限定公開
Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
Availability of remote photoduplication service: 可
Periodical Title (URI): http://hdl.handle.net/10191/51320
Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション
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