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Astrocytic control of behavior by optogenetic GPCR activation

Research Project

Project/Area Number 15K14326
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Neurophysiology / General neuroscience
Research InstitutionInstitute of Physical and Chemical Research

Principal Investigator

Iwai Youichi  国立研究開発法人理化学研究所, 脳科学総合研究センター, 研究員 (40332332)

Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywordsグリア光遺伝学 / Gタンパク質共役型受容体(GPCR) / アストロサイト / グリア-ニューロン相互作用 / 記憶・学習 / 情動 / 神経調節物質 / 新規環境 / G蛋白質共役型受容体(GPCR) / グリア-ニューロン相互作用
Outline of Final Research Achievements

Astrocytes exhibit prominent and synchronized Ca2+ elevations in wide cortical regions in response to salient stimulations. This Ca2+ elevation is Gq-type adrenergic receptor-dependent and represents a major astrocytic Ca2+ signal in awake conditions. However, its impact on animals’ behavior remains unknown.
To directly address this issue, we generated transgenic mice in which an optically activatable Gq-GPCR is selectively expressed in astrocytes and confirmed that astrocytic Ca2+ elevation was triggered by brief light illumination. Transient astrocytic Gq-activation inhibited neuronal activity and reduced locomotor activity via adenosine A1 receptor. Optogenetic activation in anterior cortex enhanced long-term object recognition memory, whereas short-term memory was not affected. These phenotypes resemble effects induced by novel-experience. Thus, astrocytic Gq-activation may represent a novelty-driven signal that is sufficient to induce behavioral adaptation to novel events.

Academic Significance and Societal Importance of the Research Achievements

集中時や新規環境下で放出されるノルアドレナリン等の神経調節物質はアストロサイトのGPCRを強く活性化することから、アストロサイトが情動や記憶を制御する可能性が示唆されている。しかしながら、これらのGPCR群はニューロンでも発現しているため、アストロサイト特異的な機能は不明であった。
本研究は高い時間・空間制御能をもつ光遺伝学的手法でこの課題に取り組み、アストロサイトのGq型GPCRシグナルが新規環境への適応を促進し、長期記憶を増強することを示唆した。アストロサイト内のGPCRシグナルは加齢や神経疾患で異常になることが示唆されており、本研究で得られた新知見は社会的な意義も大きい。

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • Research Products

    (4 results)

All 2016 2015 Other

All Journal Article (2 results) (of which Int'l Joint Research: 1 results,  Peer Reviewed: 1 results,  Open Access: 1 results,  Acknowledgement Compliant: 1 results) Presentation (1 results) (of which Int'l Joint Research: 1 results) Remarks (1 results)

  • [Journal Article] Calcium imaging reveals glial involvement in transcranial direct current stimulation-induced plasticity in mouse brain2016

    • Author(s)
      H Monai, M Ohkura, M Tanaka, Y Oe, A Konno, H Hirai, K Mikoshiba, S Itohara, J Nakai, Y Iwai & H Hirase
    • Journal Title

      Nature communications

      Volume: 7 Issue: 1 Pages: 11100-11100

    • DOI

      10.1038/ncomms11100

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] 拡散性伝達によるアストロサイトの活性化2015

    • Author(s)
      岩井陽一、 平瀬肇
    • Journal Title

      生体の科学

      Volume: 66 Pages: 551-554

    • Related Report
      2015 Research-status Report
  • [Presentation] Rapid astrocytic control of neural activity by optogenetic Gq-coupled receptor activation in vivo2016

    • Author(s)
      Youichi Iwai, Katsuya Ozawa, Kazuko Yahagi, Shunsuke Sato and Hajime Hirase
    • Organizer
      Society for Neuroscience 46th annual meeting
    • Place of Presentation
      San Diego (USA)
    • Year and Date
      2016-11-12
    • Related Report
      2016 Annual Research Report
    • Int'l Joint Research
  • [Remarks] 微弱な電気刺激が脳を活性化する仕組みを解明-ノルアドレナリンを介したアストロサイトの活動が鍵-

    • URL

      http://www.riken.jp/pr/press/2016/20160322_1/

    • Related Report
      2015 Research-status Report

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Published: 2015-04-16   Modified: 2020-03-30  

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