NAKAJIMA, Kazunori



School of Medicine, Department of Anatomy (Shinanomachi)



E-mail Address

E-mail address

Related Websites

Contact Address

35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan

External Links

Career 【 Display / hide

  • 1988.05

    Keio University Hospital, Department of Internal Medicine, Resident physician

  • 1994.04

    the University of Tokyo (Professor Katsuhiko Mikoshiba), Postdoctoral Research Fellow of the Japan Society for the Promotion of Science

  • 1994.04

    Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Molecular Neurobiology Laboratory (Chief Scientist: Dr. Katsuhiko Mikoshiba), Research Collaborative Advisor,

  • 1995.04

    Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Molecular Neurobiology Laboratory, Research Scientist

  • 1996.02

    St. Jude Children’s Research Hospital, Memphis, U.S.A., Department of Developmental Neurobiology (Chairman: Dr. Tom Curran), Visiting Scientist

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Academic Background 【 Display / hide

  • 1982.04

    Keio University, School of Medicine

    University, Graduated

  • 1990.04

    Osaka University, Graduate School, Division of Medicine, 生理系

    Graduate School, Graduated, Doctoral course

Academic Degrees 【 Display / hide

  • Ph.D., Osaka University, Coursework, 1994.03

Licenses and Qualifications 【 Display / hide

  • M.D., 1988.06


Research Areas 【 Display / hide

  • Developmental biology (Developmental neurobiology)

Research Keywords 【 Display / hide

  • 中枢神経系の組織構築機構

  • 神経細胞移動

  • 脳皮質形成機構

Research Themes 【 Display / hide

  • Mechanisms of cerebral cortical development, 



Books 【 Display / hide

  • Comprehensive Developmental Neuroscience: Cellular Migration and Formation of Axons and Dendrites, 2nd Edition

    Kanehiro Hayashi, Katsutoshi Sekine, Hidenori Tabata, and Kazunori Nakajima., Elsevier, 2020,  Page: 289-304

  • ヒトの脳は、何が特別なのか?、『特別展 人体 神秘への挑戦』

    吉永怜史、仲嶋 一範, NHK・NHKプロモーション・朝日新聞社, 2018.03,  Page: 183

    Contact page: 172-176

  • 大脳皮質の層形成機構 、『再生医療シリーズ:脳神経系の再生医学 —発生と再生の融合的新展開—(井村裕夫・高橋淳 監修、河崎洋志 編集) 』

    仲嶋 一範, 診断と治療社 , 2015.01,  Page: 169

    Contact page: 60-65

  • ニューロンの移動と層および神経核の形成、『脳の発生学 ニューロンの誕生・分化・回路形成(宮田卓樹・山本亘彦 編)』

    仲嶋 一範, 化学同人, 2013.06

    Scope: 53-71

  • Cell polarity and initiation of migration (Chapter 12). Comprehensive Developmental Neuroscience: Cellular Migration and Formation of Neuronal Connections (J.L.R. Rubenstein, P. Rakic, ed.)

    Katsutoshi Sekine, Hidenori Tabata, and Kazunori Nakajima* (* is the corresponding author), Amsterdam, Academic Press, 2013.05,  Page: 1080

    Contact page: 231-244

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Papers 【 Display / hide

  • VLDLR is not essential for Reelin-induced neuronal aggregation but suppresses neuronal invasion into the marginal zone.(Selected to appear as a Research Highlight)

    Hirota, Y. ,Nakajima,K.

    Development  2020.06

    Research paper (scientific journal), Joint Work, Accepted

  • Neuron-derived VEGF contributes to cortical and hippocampal development independently of VEGFR1/2-mediated neurotrophism.

    Keisuke Okabe, Hugh Fukada, Ikue Tai-Nagara, Tomofumi Ando, Takao Honda, Kazunori Nakajima, Norihiko Takeda, Guo-Hua Fong, Masatsugu Ema, and Yoshiaki Kubota

    Dev. Biol. (Dev. Biol.)  459 ( 2 ) 65 - 71 2020.03

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  00121606

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    © 2019 The Authors Vascular endothelial growth factor (VEGF) is a potent mitogen critical for angiogenesis and organogenesis. Deletion or inhibition of VEGF during development not only profoundly suppresses vascular outgrowth, but significantly affects the development and function of various organs. In the brain, VEGF is thought to not only promote vascular growth, but also directly act on neurons as a neurotrophic factor by activating VEGF receptors. In the present study, we demonstrated that deletion of VEGF using hGfap-Cre line, which recombines genes specifically in cortical and hippocampal neurons, severely impaired brain organization and vascularization of these regions. The mutant mice had motor deficits, with lethality around the time of weaning. Multiple reporter lines indicated that VEGF was highly expressed in neurons, but that its cognate receptors, VEGFR1 and 2 were exclusive to endothelial cells in the brain. In accordance, mice lacking neuronal VEGFR1 and VEGFR2 did not exhibit neuronal deformities or lethality. Taken together, our data suggest that neuron-derived VEGF contributes to cortical and hippocampal development likely through angiogenesis independently of direct neurotrophic effects mediated by VEGFR1 and 2.

  • Drebrin-like (Dbnl) controls neuronal migration via regulating N-cadherin expression in the developing cerebral cortex

    Seika Inoue, Kanehiro Hayashi, Kyota Fujita, Kazuhiko Tagawa, Hitoshi Okazawa, Ken-ichiro Kubo, and Kazunori Nakajima* (*corresponding author)

    J. Neurosci. (Journal of Neuroscience)  39 ( 4 ) 678 - 691 2019.01

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  02706474

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    © 2019 the authors. The actin cytoskeleton is crucial for neuronal migration in the mammalian developing cerebral cortex. The adaptor protein Drebrin-like (Dbnl) plays important roles in reorganization of the actin cytoskeleton, dendrite formation, and endocytosis by interacting with F-actin, cobl, and dynamin. Although Dbnl is known to be expressed in the brain, the functions of this molecule during brain development are largely unknown. In this study, to examine the roles of Dbnl in the developing cerebral cortex, we conducted experiments using mice of both sexes with knockdown of Dbnl, effected by in utero electroporation, in the migrating neurons of the embryonic cortex. Time-lapse imaging of the Dbnl-knockdown neurons revealed that the presence of Dbnl is a prerequisite for appropriate formation of processes in the multipolar neurons in the multipolar cell accumulation zone or the deep part of the subventricular zone, and for neuronal polarization and entry into the cortical plate. We found that Dbnl knockdown decreased the amount of N-cadherin protein expressed on the plasma membrane of the cortical neurons. The defect in neuronal migration caused by Dbnl knockdown was rescued by moderate overexpression of N-cadherin and αN-catenin or by transfection of the phospho-mimic form(Y337E, Y347E), but not the phospho-resistant form(Y337F, Y347F), of Dbnl. These results suggest that Dbnl controls neuronal migration, neuronal multipolar morphology, and cell polarity in the developing cerebral cortex via regulating N-cadherin expression.

  • Both excitatory and inhibitory neurons transiently form clusters at the outermost region of the developing mammalian cerebral neocortex

    Minkyung Shin, Ayako Kitazawa, Satoshi Yoshinaga, Kanehiro Hayashi, Yukio Hirata, Colette Dehay, Ken-ichiro Kubo*, and Kazunori Nakajima* (*corresponding authors)(M. Shin and A. Kitazawa are co-first authors)

    J. Comp. Neurol. (Journal of Comparative Neurology)  527 ( 10 ) 1577 - 1597 2019

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  00219967

     View Summary

    © 2019 Wiley Periodicals, Inc. During development of the mammalian cerebral neocortex, postmitotic excitatory neurons migrate toward the outermost region of the neocortex. We previously reported that this outermost region is composed of densely packed relatively immature neurons; we named this region, which is observed during the late stage of mouse neocortical development, the “primitive cortical zone (PCZ).” Here, we report that postmigratory immature neurons spend about 1–1.5 days in the PCZ. An electron microscopic analysis showed that the neurons in the PCZ tend to be in direct contact with each other, mostly in a radial direction, forming “primitive neuronal clusters” with a height of 3–7 cells and a width of 1–2 cells. A time-course analysis of fluorescently labeled neurons revealed that the neurons took their positions within the primitive clusters in an inside-out manner. The neurons initially participated in the superficial part of the clusters, gradually shifted their relative positions downward, and then left the clusters at the bottom of this structure. GABAergic inhibitory interneurons were also found within the primitive clusters in the developing mouse neocortex, suggesting that some clusters are composed of both excitatory neurons and inhibitory interneurons. Similar clusters were also observed in the outermost region of embryonic day (E) 78 cynomolgus monkey occipital cortex and 23 gestational week (GW) human neocortices. In the primate neocortices, including human, the presumptive primitive clusters seemed to expand in the radial direction more than that observed in mice, which might contribute to the functional integrity of the primate neocortex.

  • Role of the immune system in the development of the central nervous system.

    Keiko Morimoto and Kazunori Nakajima* (*corresponding author)

    Front. Neurosci. (Frontiers in Neuroscience)  13 2019

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  16624548

     View Summary

    © Copyright © 2019 Morimoto and Nakajima. The central nervous system (CNS) and the immune system are both intricate and highly organized systems that regulate the entire body, with both sharing certain common features in developmental mechanisms and operational modes. It is known that innate immunity-related molecules, such as cytokines, toll-like receptors, the complement family, and acquired immunity-related molecules, such as the major histocompatibility complex and antibody receptors, are also expressed in the brain and play important roles in brain development. Moreover, although the brain has previously been regarded as an immune-privileged site, it is known to contain lymphatic vessels. Not only microglia but also lymphocytes regulate cognition and play a vital role in the formation of neuronal circuits. This review provides an overview of the function of immune cells and immune molecules in the CNS, with particular emphasis on their effect on neural developmental processes.

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Papers, etc., Registered in KOARA 【 Display / hide

Reviews, Commentaries, etc. 【 Display / hide

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Presentations 【 Display / hide

  • Analysis of extrinsic signals for layer 4 subtype specification in the neocortex


    第43回日本神経科学大会 (神戸コンベンションセンター(兵庫県神戸市)<オンライン/誌上開催に変更>) , 2020.07, Poster (general)

  • Two-photon voltage imaging of spontaneous activity from multiple neurons reveals network activity in brain tissue

    Binglun Li, Mariya Chavarha, Yuho Kobayashi, Satoshi Yoshinaga, Kazunori Nakajima, Michael Z. Lin, Takafumi Inoue

    第43回日本神経科学大会 (神戸コンベンションセンター(兵庫県神戸市)<オンライン/誌上開催に変更>) , 2020.07, Poster (general)

  • Analysis of HA-tagged-Dab1-expressing mice using CRISPR/Cas9-mediated genome editing


    第43回日本神経科学大会 (神戸コンベンションセンター(兵庫県神戸市)<オンライン/誌上開催に変更>) , 2020.07, Poster (general)

  • Transcriptional networks to specify subcortical projection neurons in subtype reprogramming


    第43回日本神経科学大会 (神戸コンベンションセンター(兵庫県神戸市)<オンライン/誌上開催に変更>) , 2020.07, Oral Presentation(general)

  • リーリン受容体VLDLRは発生中の大脳皮質において辺縁帯内へのニューロンの進入を阻止する


    第125回日本解剖学会総会・全国学術集会  (ANAクラウンプラザホテル宇部(山口県宇部市)<誌上開催に変更>) , 2020.03, Poster (general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 場との連携による脳細胞の動態制御機構


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Kazunori Nakajima, Grant-in-Aid for Scientific Research

  • 成熟した大脳皮質神経細胞のサブタイプを生体内で人為的に転換させる試み


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Kazunori Nakajima, Grant-in-Aid for Challenging Exploratory Research, Principal Investigator

  • 大脳皮質構造の形成機構


    慶應義塾福澤基金委員会, 福澤基金研究補助, Kazunori Nakajima, Other, Principal Investigator

  • 神経細胞の生存を守る内在性機構の解明


    Takeda Science Foundation, 武田科学振興財団 ビジョナリーリサーチ研究助成, Kazunori Nakajima, Commissioned research, Principal Investigator

  • 脳の構造が整然と作られるメカニズムの解明


    Takeda Science Foundation, 武田科学振興財団 生命科学研究助成, Kazunori Nakajima, Commissioned research, Principal Investigator

Awards 【 Display / hide

  • 第29回(2012年度)井上学術賞

    Kazunori Nakajima, 2013.02, 井上科学振興財団, 大脳皮質の発生・分化機構

    Type of Award: Awards of Publisher, Newspaper Company and Foundation.  Country: Japan

  • 第5回上田英雄賞

    2001.04, 東京慈恵会医科大学やよい会, 脳神経細胞の配置決定のメカニズム

    Type of Award: Other Awards.  Country: 日本

  • The Award for Distinguished Young Investigator

    Kazunori Nakajima, 2000.10, Japanese Society for Neurochemistry, 脳皮質形成のメカニズム

    Type of Award: Awards of National Conference, Council and Symposium


Courses Taught 【 Display / hide

  • 神経解剖学




  • 肉眼解剖学


  • 骨学


  • 自主学習


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Courses Previously Taught 【 Display / hide

  • 生物科学特別講義Ⅱ

    東京大学理学部生物学科, 2020

  • 分子細胞生物学(MCB)

    慶応義塾大学医学部, 2020

  • 生物学特論

    慶応義塾大学医学部, 2020

  • 自主学習

    慶応義塾大学医学部, 2020

  • 骨学

    慶応義塾大学医学部, 2020

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Educational Activities and Special Notes 【 Display / hide

  • 2020年 慶應義塾大学医学教育貢献賞(Outstanding teacher award)


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  • 第15回慶應義塾大学医学部ベスト・ティーチャー賞


  • 第14回慶應義塾大学医学部ベスト・ティーチャー賞


    , Device of Educational Contents

  • 第13回慶應義塾大学医学部ベスト・ティーチャー賞


    , Device of Educational Contents

  • 第12回慶應義塾大学医学部ベスト・ティーチャー賞


    , Device of Educational Contents

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Social Activities 【 Display / hide

  • 第42回四谷祭(慶應義塾大学信濃町キャンパス学園祭)にて一般向け研究室ツアー

  • 第41回四谷祭(慶應義塾大学信濃町キャンパス学園祭)にて一般向け研究室ツアー

  • 特別展「人体 ―神秘への挑戦―」(国立科学博物館)にて脳に関する展示に協力


  • 第40回四谷祭(慶應義塾大学信濃町キャンパス学園祭)にて一般向け研究室ツアー

  • 慶應義塾大学医学部解剖学教室仲嶋研究室オープンラボ2017


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Memberships in Academic Societies 【 Display / hide

  • 日本神経化学会

  • 日本発生生物学会

  • 日本解剖学会

  • 日本分子生物学会

  • 日本神経科学学会


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Committee Experiences 【 Display / hide

  • 2002.06

    Editorial Advisory Board Member, The Keio Journal of Medicine

  • 2002.12

    Editorial Board Member, Developmental Brain Research (Elsevier)

  • 2004.01

    Editorial Board Member, Molecular and Cellular Biochemistry

  • 2009.01

    Review Editor, Frontiers in Neuroanatomy

  • 2009.07

    Review Editor for Specialty Section Neurogenesis, Frontiers in Neuroscience

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