Updated on 2022/05/26

写真a

 
SAKURAGI, Shigeo
 
Affiliation
Faculty of Science and Engineering, School of Advanced Science and Engineering
Job title
Assistant Professor(non-tenure-track)

Education

  • 2010.04
    -
    2014.09

    Osaka University   Graduate School of Frontier Biosciences  

Research Experience

  • 2022.04
    -
    Now

    Waseda University   Faculty of Science and Engineering, School of Advanced Science and Engineering   Assistant Professor

  • 2020.04
    -
    2022.03

    Waseda University   Research Institute for Science and Engineering   Junior Researcher

  • 2018.04
    -
    2020.03

    Yamagata University   Faculty of Medicine School of Medicine   Assistant Professor

  • 2016.04
    -
    2018.03

    Tohoku University   Graduate School of Life Sciences   Specially Appointed Assistant Professor

  • 2014.10
    -
    2016.03

    Nagoya University   Graduate School of Science   Postdoctral fellow

Professional Memberships

  •  
     
     

    THE PHYSIOLOGICAL SOCIETY OF JAPAN

  •  
     
     

    THE JAPAN NEUROSCIENCE SOCIETY

 

Research Areas

  • Pharmacology

  • Physiology

  • Neuroscience-general

Research Interests

  • Synaptic Plasticity

  • Memory

  • BDNF

  • Hippocampus

  • Astrocyte

  • Electrophysiology

  • single particle tracking

  • Calcium imaging

  • Optogenetics

▼display all

Papers

  • Inhibitory Synaptic Transmission Tuned by Ca2+ and Glutamate Through the Control of GABAAR Lateral Diffusion Dynamics

    Bannai H, Niwa F, Sakuragi S, Mikoshiba K

    Dev. Growth Differ.   62 ( 6 ) 398 - 406  2020.04  [Refereed]

    DOI

  • Optogenetic study of the response interaction among multi-afferent inputs in the barrel cortex of rats

    Liu Y, Ohshiro T, Sakuragi S, Koizumi K, Mushiake H, Ishizuka T, Yawo H

    Sci. Rep.   9 ( 1 ) 3917  2019.03  [Refereed]

    DOI

  • Astroglial Ca2+ signaling is generated by the coordination of IP3R and store-operated Ca2+ channels

    Sakuragi S, Niwa F, Oda Y, Mikoshiba K, Bannai H

    Biochem. Biophys. Res. Commun.   486 ( 4 ) 879 - 885  2017.05  [Refereed]

    Authorship:Lead author

     View Summary

    Astrocytes play key roles in the central nervous system and regulate local blood flow and synaptic transmission via intracellular calcium (Ca2+) signaling. Astrocytic Ca2+ signals are generated by multiple pathways: Ca2+ release from the endoplasmic reticulum (ER) via the inositol 1, 4, 5-trisphosphate receptor (IP3R) and Ca2+ influx through various Ca2+ channels on the plasma membrane. However, the Ca2+ channels involved in astrocytic Ca2+ homeostasis or signaling have not been fully characterized. Here, we demonstrate that spontaneous astrocytic Ca2+ transients in cultured hippocampal astrocytes were induced by cooperation between the Ca2+ release from the ER and the Ca2+ influx through store-operated calcium channels (SOCCs) on the plasma membrane. Ca2+ imaging with plasma membrane targeted GCaMP6f revealed that spontaneous astroglial Ca2+ transients were impaired by pharmacological blockade of not only Ca2+ release through IP(3)Rs, but also Ca2+ influx through SOCCs. Loss of SOCC activity resulted in the depletion of ER Ca2+, suggesting that SOCCs are activated without store depletion in hippocampal astrocytes. Our findings indicate that sustained SOCC activity, together with that of the sarco-endoplasmic reticulum Ca2+-ATPase, contribute to the maintenance of astrocytic Ca2+ store levels, ultimately enabling astrocytic Ca2+ signaling. (C) 2017 Elsevier Inc. All rights reserved.

    DOI

  • Kinetic characteristics of chimeric channelrhodopsins implicate the molecular identity involved in desensitization

    Zamani A*, Sakuragi S* (*equal contribution), Ishizuka T, Yawo H

    Biophys. Physicobiol.   14   13 - 22  2017.01  [Refereed]

    Authorship:Lead author

    DOI

  • Dissection of local Ca2+ signals inside cytosol by ER-targeted Ca2+ indicator

    Niwa F, Sakuragi S, Kobayashi A, Takagi S, Oda Y, Bannai H, Mikoshiba K

    Biochem. Biophys. Res. Comm.   479 ( 1 ) 67 - 73  2016.10  [Refereed]

     View Summary

    Calcium (Ca2+) is a versatile intracellular second messenger that operates in various signaling pathways leading to multiple biological outputs. The diversity of spatiotemporal patterns of Ca2+ signals, generated by the coordination of Ca2+ influx from the extracellular space and Ca2+ release from the intracellular Ca2+ store the endoplasmic reticulum (ER), is considered to underlie the diversity of biological outputs caused by a single signaling molecule. However, such Ca2+ signaling diversity has not been well described because of technical limitations. Here, we describe a new method to report Ca2+ signals at subcellular resolution. We report that OER-GCaMP6f, a genetically encoded Ca2+ indicator (GECI) targeted to the outer ER membrane, can monitor Ca2+ release from the ER at higher spatiotemporal resolution than conventional GCaMP6f. OER-GCaMP6f was used for in vivo Ca2+ imaging of C elegans. We also found that the spontaneous Ca2+ elevation in cultured astrocytes reported by OER-GCaMP6f showed a distinct spatiotemporal pattern from that monitored by plasma membrane-targeted GCaMP6f (Lck-GCaMP6f); less frequent Ca2+ signal was detected by OER-GCaMP6f, in spite of the fact that Ca2+ release from the ER plays important roles in astrocytes. These findings suggest that targeting of GECI5 to the ER outer membrane enables sensitive detection of Ca2+ release from the ER at subcellular resolution, avoiding the diffusion of GECI and Ca2+. Our results indicate that Ca2+ imaging with OER-GCaMP6f in combination with Lck-GCaMP6f can contribute to describing the diversity of Ca2+ signals, by enabling dissection of Ca2+ signals at subcellular resolution. (C) 2016 Elsevier Inc. All rights reserved.

    DOI

  • Dendritic spine dynamics leading to spine elimination after repeated inductions of LTD

    Sho Hasegawa, Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    SCIENTIFIC REPORTS   5   7707  2015.01  [Refereed]

     View Summary

    Memory is fixed solidly by repetition. However, the cellular mechanism underlying this repetition-dependent memory consolidation/reconsolidation remains unclear. In our previous study using stable slice cultures of the rodent hippocampus, we found long-lasting synaptic enhancement/suppression coupled with synapse formation/elimination after repeated inductions of chemical LTP/LTD, respectively. We proposed these phenomena as useful model systems for analyzing repetition-dependent memory consolidation. Recently, we analyzed the dynamics of dendritic spines during development of the enhancement, and found that the spines increased in number following characteristic stochastic processes. The current study investigates spine dynamics during the development of the suppression. We found that the rate of spine retraction increased immediately leaving that of spine generation unaltered. Spine elimination occurred independent of the pre-existing spine density on the dendritic segment. In terms of elimination, mushroom-type spines were not necessarily more stable than stubby-type and thin-type spines.

    DOI

  • Involvement of TrkB- and p75NTR -signaling pathways in two contrasting forms of long-lasting synaptic plasticity

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    Scientific Reports   3   3185  2013  [Refereed]

    Authorship:Lead author

     View Summary

    The repetition of experience is often necessary to establish long-lasting memory. However, the cellular mechanisms underlying this repetition-dependent consolidation of memory remain unclear. We previously observed in organotypic slice cultures of the rodent hippocampus that repeated inductions of long-term potentiation (LTP) led to a slowly developing long-lasting synaptic enhancement coupled with synaptogenesis. We also reported that repeated inductions of long-term depression (LTD) produced a long-lasting synaptic suppression coupled with synapse elimination. We proposed these phenomena as useful in vitro models for analyzing repetition-dependent consolidation. Here, we hypothesized that the enhancement and suppression are mediated by the brain-derived neurotrophic factor (BDNF)-TrkB signaling pathway and the proBDNF-p75 NTR pathway, respectively. When we masked the respective pathways, reversals of the enhancement and suppression resulted. These results suggest the alternative activation of the p75 NTR pathway by BDNF under TrkB-masking conditions and of the TrkB pathway by proBDNF under p75 NTR -masking conditions, thus supporting the aforementioned hypothesis.

    DOI PubMed

  • Involvement of the p75(NTR) Signaling Pathway in Persistent Synaptic Suppression Coupled With Synapse Elimination Following Repeated Long-Term Depression Induction

    Yoshihiro Egashira, Tsunehiro Tanaka, Priyanka Soni, Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    JOURNAL OF NEUROSCIENCE RESEARCH   88 ( 16 ) 3433 - 3446  2010.12  [Refereed]

     View Summary

    Synaptic plasticity, especially structural plasticity, is thought to be a basis for long-lasting memory. We previously reported that, in rat hippocampus slice cultures, repeated induction of long-term depression (LTD) by application of a metabotropic glutamate receptor (mGluR) agonist led to slowly developing, long-lasting synaptic suppression coupled with synapse elimination. We referred to this phenomenon as LOSS (LTD-repetition-operated synaptic suppression) to discriminate it from conventional single LTD and proposed it as a model for analyzing structural plasticity. Recently, proneurotrophin-activated p75(NTR) signaling has been gaining attention as a possible pathway for the regulation of both neuronal apoptosis and synaptic plasticity. In this study, we examined whether this signaling has a role in the establishment of LOSS. The application of anisomycin indicated that, for LOSS to occur, novel protein synthesis is needed within 6 hr after the induction of mGluR-dependent LTD, which demonstrates that LOSS is an active process and therefore is not due to withering in response to a shortage of trophic factors. Furthermore, we found that pro-BDNF (a species of proneurotrophins) is newly synthesized within 6 hr after the induction of LTD. We therefore exogenously applied a cleavage-resistant form of pro-BDNF, finding synaptic suppression similar to LOSS. LOSS could be abolished by the application of an antibody that binds to and neutralizes p75(NTR) following repeated LTD induction. These results suggest involvement of the p75(NTR) signaling pathway in the for g-lasting decremental form of synaptic plasticity. (C) 2010 Wiley-Liss, Inc.

    DOI

▼display all

Awards

  • 5th Biophysics and Physicobioloby Editors' Choice Award

    2018.07  

Presentations

  • DNAを介した量子ドット1分子イメージングによる膜脂質の動態解析

    櫻木繁雄, 片桐太郎, 李銘哲, 坂内博子

    第11回日本生物物理学会関東支部会 

    Presentation date: 2022.03

  • タウオリゴマー光誘導モデル細胞を用いたタウオリゴマーの継時的推移

    櫻木繁雄, 松本弦, 添田義行, 吉村英哲, 高島明彦, 坂内博子

    シンギュラリティ生物学第6回領域会議 

    Presentation date: 2022.01

  • The diffusion dynamics and the distribution of GABAA receptor influenced by the isoflurane administration.

    Shigeo Sakuragi, Junichiro Ono, Hiroko Bannai

    The 44th Annual Meeting of the Japan Neuroscience Society 

    Presentation date: 2021.07

  • Influence of volatile anesthetics on GABAA receptor diffusion dynamics

    Shigeo Sakuragi, Taro Katagiri, Junichiro Ono, Hiroko Bannai

    194th Japanese-French Biology Society regular meeting 

    Presentation date: 2021.06

  • Induction of astroglial Ca2+ signaling by IP3R-SOC coordinated system

    Shigeo Sakuragi, Fumihiro Niwa, Yoichi Oda, Hiroko Bannai, Katsuhiko Mikoshiba

    The 94th Annual Meeting of the Physiological Society of Japan  (Hamamatsu) 

    Presentation date: 2017.03

  • The role of Store-Operated Ca2+ channel in astroglial Ca2+ signaling

    Shigeo Sakuragi, Fumihiro Niwa, Yoichi Oda, Hiroko Bannai, Katsuhiko Mikoshiba

    Physiological society of Tohoku region 48th meeting 

    Presentation date: 2016.10

  • Further evidence for the involvement of BDNF/proBDNF signaling in long-lasting synaptic plasticity

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    The 57th Annual Meeting of the Japanese Society of Neurochemistry 

    Presentation date: 2014.10

  • The involvement of TrkB and p75NTR pathways in two opposite forms of the synaptic plasticity.

    Shigeo Sakuragi

    The 93th Colloquium of Graduate School of Frontier Biosciences  (Osaka) 

    Presentation date: 2013.11

  • Two opposite forms of long-lasting synaptic plasticity explained by the effects of BDNF and its precursor

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    The 36th Annual Meeting of the Japan Neuroscience Society 

    Presentation date: 2013.06

  • Synapse generation/inhibition and BDNF/proBDNF signaling after repetitive induction of LTP/LTD

    Shigeo Sakuragi

    NIPS Research meetings 2012  (Okazaki) 

    Presentation date: 2012.11

  • Two opposite forms of long-lasting synaptic plasticity explained by yin-yang effects of BDNF and its precursor

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    Society for Neuroscience 42th Annual Meeting 

    Presentation date: 2012.10

  • Involvement of the BDNF-TrkB signaling pathway in the long-lasting synaptic plasticity in hippocampal slice cultures

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    The 35th Annual Meeting of the Japan Neuroscience Society 

    Presentation date: 2012.09

  • Release of BDNF in long-lasting synaptic enhancement of cultured hippocampal slices

    Shigeo Sakuragi, Keiko Tominaga-Yoshino, Akihiko Ogura

    The 54th Annual Meeting of the Japanese Society of Neurochemistry 

    Presentation date: 2011.09

▼display all

 

Syllabus

▼display all

Teaching Experience

  • Human body structure and disease

    Yamagata University  

    2019
    -
     
     

  • Laboratory Study

    Yamagata University Faculty of Medicine  

    2018
    -
    2019
     

  • Pharmacology

    Yamagata University Faculty of Medicine  

    2018
    -
    2019