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Regulation of social behavior by reciprocal interaction between OXTergic and DAergic system

Research Project

Project/Area Number 16K01954
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Basic / Social brain science
Research InstitutionSaitama Medical University (2018-2019)
Kyorin University (2016-2017)

Principal Investigator

Fujiwara Tomonori  埼玉医科大学, 保健医療学部, 教授 (90255399)

Project Period (FY) 2016-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywordsシナプス関連タンパク質 / シンタキシン / 開口放出 / 社会行動 / ドパミン / オキシトシン / シナプス関連蛋白質 / シナプス関連 / シナプス関連分子 / 神経科学 / 行動学
Outline of Final Research Achievements

STX1A is known to regulate synaptic vesicle exocytosis. We found that STX1A gene might be implicated in autistic spectrum disorder. In STX1A gene knockout mice (STX1A KO), unusual behavioral properties including impairment of social recognition memory was observed. We demonstrated that STX1A KO exhibited reduction of oxytocin (OXT) release in CNS. We analyzed the regulation of social behavior by OXT using STX1A KO as a model animals. We found that the effect of OXT was related with DAergic system, and reciprocal interaction between OXTergic and DAergic system played important roles for regulation of social behavior.

Academic Significance and Societal Importance of the Research Achievements

近年の研究で、ヒト精神神経疾患にシナプス関連分子が関連することが明らかになってきた。本研究では、神経伝達物質の放出を制御するSTX1Aが自閉性疾患に関連することを示した。また、STX1Aを欠損させたマウスをモデルとして、自閉性疾患でみられる病態を引き起こす分子機構について検討を行った。そのため、本研究はヒト精神神経疾患の病態解明に向けた有意義な研究である。

Report

(5 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (17 results)

All 2020 2019 2018 2017 2016

All Journal Article (4 results) (of which Peer Reviewed: 4 results,  Open Access: 1 results,  Acknowledgement Compliant: 1 results) Presentation (13 results) (of which Int'l Joint Research: 6 results)

  • [Journal Article] A part of patients with autism spectrum disorder has haploidy of HPC-1/syntaxin1A gene that possibly caused behavioral disturbance as in experimentally gene ablated mice.2017

    • Author(s)
      Kofuji T, Hayashi Y, Fujiwara T, Sanada M, Tamaru M, Akagawa K
    • Journal Title

      Neuroscience letters

      Volume: 644 Pages: 5-9

    • DOI

      10.1016/j.neulet.2017.02.052

    • Related Report
      2017 Research-status Report
    • Peer Reviewed
  • [Journal Article] Syntaxin 1B contributes to regulation of the dopaminergic system through GABA transmission in the CNS.2017

    • Author(s)
      Fujiwara T, Kofuji T, Mishima T, Akagawa K
    • Journal Title

      Eur J Neurosci.

      Volume: 46 Issue: 12 Pages: 2867-2874

    • DOI

      10.1111/ejn.13779

    • Related Report
      2017 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] A part of patients with autism spectrum disorder has haploidy of HPC-1/syntaxin1A gene that possibly causes behavioral disturbance as in experimentally gene ablated mice.2017

    • Author(s)
      Kofuji T, Hayashi Y, Fujiwara T, Sanada M, Tamaru M, Akagawa K.
    • Journal Title

      Neurosci Lett.

      Volume: 644 Pages: 5-9

    • Related Report
      2016 Research-status Report
    • Peer Reviewed
  • [Journal Article] Unusual social behavior in HPC-1/syntaxin1A knockout mice is caused by disruption of the oxytocinergic neural system2016

    • Author(s)
      T Fujiwara, M Sanada, T Kofuj and K Akagawa
    • Journal Title

      J Neurochem

      Volume: 138 Issue: 1 Pages: 117-23

    • DOI

      10.1111/jnc.13634

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Acknowledgement Compliant
  • [Presentation] Syntaxin1A knockout mice showed unusual social behavior in their homecage.2020

    • Author(s)
      T Fujiwara, T Kofuji, T Furukawa and K Akagawa
    • Organizer
      FENS2020
    • Related Report
      2019 Annual Research Report
    • Int'l Joint Research
  • [Presentation] Role of syntaxin1B in GABA-mediated regulation of network activities: Behavioral and neuronal analysis of fever-associated epilepsy syndromes in syntaxin1B gene-ablated mice2019

    • Author(s)
      T Mishima, T Fujiwara, T Kofuji, A Saito, Y Terao and K Akagawa
    • Organizer
      日本神経科学
    • Related Report
      2019 Annual Research Report
  • [Presentation] Seizure phenotype in syntaxin1B gene knockout mice was caused by impaired GABAergic system2019

    • Author(s)
      Kofuji T, Mishima T, Fujiwara T, A Saito, Terao Y, Akagawa K
    • Organizer
      日本神経科学
    • Related Report
      2019 Annual Research Report
  • [Presentation] Unusual social behavior in HPC-1/syntaxin1A knockout mice2018

    • Author(s)
      T Fujiwara, T Kofuji, T Mishima, Y Terao and K Akagawa
    • Organizer
      日本生理学会
    • Related Report
      2018 Research-status Report
  • [Presentation] Syntaxin1B contributes to regulation of the dopaminergic system through GABA transmission in the CNS.2018

    • Author(s)
      T Fujiwara, T Kofuji, T Mishima, Y Terao and K Akagawa
    • Organizer
      11th FENS Forum of Neuroscience
    • Related Report
      2018 Research-status Report
    • Int'l Joint Research
  • [Presentation] HPC-1/syntaxin 1A regulates the cortical signal propagation by affecting the GABAergic transmission.2018

    • Author(s)
      Osanai M, Matsumura A, Fujiwara T, Kikuta S, Yagi T, Akagawa K.
    • Organizer
      11th FENS Forum of Neuroscience
    • Related Report
      2018 Research-status Report
    • Int'l Joint Research
  • [Presentation] シンタキシン1B遺伝子欠損マウスのけいれん表現型の解析2017

    • Author(s)
      T Mishima, T Fujiwara, T Kofuji and K Akagawa
    • Organizer
      日本生理学会
    • Place of Presentation
      浜松
    • Year and Date
      2017-03-28
    • Related Report
      2016 Research-status Report
  • [Presentation] Five Cases of Autism Spectrum Disorder with Syntaxin1A Gene Haploidy2017

    • Author(s)
      Kofuji T, Hayashi Y, Fujiwara T, Sanada M, Tamaru M, and Akagawa K
    • Organizer
      AOCCN
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] T FUJIWARA, T KOFUJI, T MISHIMA, Y TERAO, and K AKAGAWA2017

    • Author(s)
      HPC-1/syntaxin1A regulates reciprocal feedforward interactions between DA and OXT systems, which, in turn, affect social behavior.
    • Organizer
      SfN
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] T Kofuji, T Fujiwara, T Mishima, Y Hayashi, M Tamaru, Y Terao and K Akagawa2017

    • Author(s)
      Disturbance of HPC-1/syntaxin1A gene expression and variation of its gene number are highly associated with autism spectrum disorder.
    • Organizer
      SfN
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] A study on the seizure phenotype of syntaxin 1B gene-ablated mice2017

    • Author(s)
      Mishima T, Fujiwara T, Kofuji T, Terao Y and Akagawa K
    • Organizer
      日本生理学会
    • Related Report
      2017 Research-status Report
  • [Presentation] A study on the behavioral and neuronal phenotype of syntaxin 1B gene-ablated mice: involvement of syntaxin 1B in the fever-associated epilepsy syndromes2017

    • Author(s)
      Mishima T, Fujiwara T, Kofuji T, Terao Y and Akagawa K
    • Organizer
      日本神経科学会
    • Related Report
      2017 Research-status Report
  • [Presentation] HPC-1/syntaxin1A is one of causative gene for autistic spectrum disorder.2016

    • Author(s)
      T Fujiwara, T Kofuji, T Mishima, Y Hayashi, M Tamaru, K Akagawa
    • Organizer
      日本神経科学会
    • Place of Presentation
      横浜
    • Year and Date
      2016-07-20
    • Related Report
      2016 Research-status Report

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Published: 2016-04-21   Modified: 2021-02-19  

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