Updated on 2026/08/25

写真a

 
KINOSHITA, Shinji
 
Affiliation
Faculty of Science and Engineering, School of Advanced Science and Engineering
Job title
Research Associate
Degree
Master of Science ( 2025.03 Waseda University )

Research Experience

  • 2025.04
    -
    Now

    Waseda University   Faculty of Science and Engineering   Research Assistant

Education Background

  • 2025.04
    -
    Now

    Waseda University   Graduate School of Advanced Science and Engineering   Department of Life Science and Medical Bioscience  

    Ph.D course

  • 2023.04
    -
    2025.03

    Waseda University   Graduate School of Advanced Science and Engineering   Department of Life Science and Medical Bioscience  

    Master course

  • 2019.04
    -
    2023.03

    Waseda University   School of Advanced Science and Engineering   Department of Life Science and Medical Bioscience  

Professional Memberships

  • 2025.08
    -
    Now

    The Japanese Society for Neurochemistry

  • 2024.02
    -
    Now

    Japan Neuroscience Society

Research Areas

  • Physiology / Cell biology / Neuroscience-general

Research Interests

  • Neuron

  • Glia

  • Astrocyte

  • Microglia

  • Oligodendrocyte

  • Calcium signal

  • ATP

  • Imaging

  • Demyelinating disease

▼display all

Awards

  • IKEDA SCIENTIFIC Award Incentive Award

    2025.09   IKEDA SCIENTIFIC Co., Ltd.   Deciphering the mechanisms underlying myelin regeneration toward applications in demyelinating disorders

 

Papers

  • δ2-Protocadherins organize parallel indirect basal ganglia circuits.

    Naosuke Hoshina, Joshua M Boeckers, Erin M Johnson-Venkatesh, Miyuki Hoshina, Kana Matsumoto, Abhijnana Das, Veronica R Rally, Jaanvi Sant, Akiko Terauchi, Shinji Kinoshita, Takafumi Inoue, Hisashi Umemori

    Science advances   12 ( 34 ) eaec8746  2026.08  [International journal]

    　View Summary

    The basal ganglia (BG) contain multiple parallel neural circuits, each of which may control different behaviors. However, how the distinct parallel BG circuits are molecularly organized is not known. Here, we show that two δ2-protocadherins (PCDHs), PCDH17 and PCDH10, which are homophilic cell adhesion molecules, establish and define two distinct indirect BG circuits that regulate different behaviors. PCDH17 and PCDH10 are expressed in a complementary expression pattern in the BG, anatomically defining two parallel indirect BG connections. Indirect pathway-specific Pcdh17 and Pcdh10 conditional knockout (cKO) mice show impaired establishment of the indirect BG circuits in a region-preferential manner. Last, the Pcdh17 cKO mice show defects in task learning, while the Pcdh10 cKO mice show defects in motor/sensory habituation. These results identify PCDH17 and PCDH10 as the molecular organizers for two distinct indirect BG circuits regulating different behaviors and reveal the molecular mechanisms for organizing parallel BG circuits.

    DOI PubMed

Misc

  • Myelin Debris Induces ATP Release and Calcium Oscillations in Astrocytes

    Shinji Kinoshita, Chihiro Adachi, Takafumi Inoue

    Society for Neuroscience    2025.11

  • Myelin fraction induces glutamate release from cultured astrocytes

    Yuki Aizawa, Shinji Kinoshita, Chihiro Adachi, Takafumi Inoue

       2025.07

  • Myelin basic protein induces ATP release and Ca oscillation in astrocytes

    Shinji Kinoshita, Chihiro Adachi, Takafumi Inoue

       2025.07

  • Myelin debris induce Calcium oscillation in cultured astrocyte

    NEURO 2024    2024.07

    J-GLOBAL

  • Myelin debris induce Calcium oscilation in cultured oligodendrocyte

    NEURO 2024    2024.07

    J-GLOBAL

 

Teaching Experience

  • Intermediate Life Science and Medical Bioscience Laboratory

    Waseda University  

    2025.09
    -
    Now
     

  • Laboratory for Advanced Science and Engineering 2B (Engineering, Advanced, JP)

    Waseda University  

    2025.09
    -
    Now
     

  • Laboratory for Advanced Science and Engineering 1A (JP)

    Waseda University  

    2025.04
    -
    Now
     

 

Internal Special Research Projects

  • 髄鞘成分によるアストロサイト活性化機構の解明と脱髄疾患病態への関与

    2025   井上貴文, 相澤雄紀

    　View Summary

    　近年、中枢神経系における脱髄病態では、グリア細胞間の相互作用が初期の病巣形成および再髄鞘化の進行に重要な役割を果たすことが明らかになってきた。しかし、脱髄発生時にどのような分子機構によって周囲の細胞応答が誘導されるのかについては、依然として未解明な点が多い。申請者はこれまでの研究から、髄鞘成分に由来する分子がアストロサイトを直接活性化し、細胞外シグナルの分泌を介して周囲の細胞に作用する可能性を見いだした。 　そこで本研究では、脱髄時に放出される髄鞘関連分子によるアストロサイト活性化機構と、その下流で誘導されるグリア細胞応答の制御機構を明らかにすることを目的とした。 　マウス由来培養グリア細胞に各種蛍光プローブを導入し、タイムラプスイメージングを用いて解析を行った。その結果、髄鞘由来成分による刺激により、アストロサイトからのATP放出が即時に誘導されることを見いだした。さらに、ATP受容体の活性化を介してグルタミン酸放出および細胞内カルシウム応答が誘導されることが明らかとなった。加えて、マウス急性脳切片での解析により、同様の反応が生体環境下においても再現されることが確認された。今後はこれらのシグナルが他の細胞種の動態や機能に及ぼす影響について検討を行う。