Updated on 2025/03/14

写真a

 
TAKEDA Ikuko
 
Organization
Graduate School of Medicine Program in Integrated Medicine Anatomy and Cell Biology Associate professor
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Associate professor
External link

Degree 1

  1. 医学(博士) ( 2014.1   広島大学 ) 

Research Interests 2

  1. neuronal circuit

  2. chronic pain

Research History 6

  1. Nagoya University   Associate professor

    2024.8

  2. Nagoya University   Department of Anatomy and Molecular Cell Biology, Gragudate School of Medicine   Lecturer

    2022.11 - 2024.7

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    Country:Japan

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  3. National Institutes of Natural Sciences, National Institute for Physiological Sciences   Division of Multicellular Circuit Dynamics

    2022.4

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  4. Nagoya University   Department of Anatomy and Molecular Cell Biology Graduate School of Medicine   Assistant Professor

    2021.9 - 2022.10

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  5. National Institutes of Natural Sciences, National Institute for Physiological Sciences   Division of Homeostatic Development

    2020.5 - 2022.3

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Education 1

  1. Hiroshima University

    2009.4 - 2014.1

 

Papers 27

  1. Controlled activation of cortical astrocytes modulates neuropathic pain-like behaviour Reviewed International coauthorship International journal

    Ikuko Takeda, Kohei Yoshihara, Dennis L. Cheung, Tomoko Kobayashi, Masakazu Agetsuma, Makoto Tsuda, Kei Eto, Schuichi Koizumi, Hiroaki Wake, Andrew J. Moorhouse, Junichi Nabekura

    Nature Communications   Vol. 13 ( 1 ) page: 4100 - 4100   2022.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    Chronic pain is a major public health problem that currently lacks effective treatment options. Here, a method that can modulate chronic pain-like behaviour induced by nerve injury in mice is described. By combining a transient nerve block to inhibit noxious afferent input from injured peripheral nerves, with concurrent activation of astrocytes in the somatosensory cortex (S1) by either low intensity transcranial direct current stimulation (tDCS) or via the chemogenetic DREADD system, we could reverse allodynia-like behaviour previously established by partial sciatic nerve ligation (PSL). Such activation of astrocytes initiated spine plasticity to reduce those synapses formed shortly after PSL. This reversal from allodynia-like behaviour persisted well beyond the active treatment period. Thus, our study demonstrates a robust and potentially translational approach for modulating pain, that capitalizes on the interplay between noxious afferents, sensitized central neuronal circuits, and astrocyte-activation induced synaptic plasticity.

    DOI: 10.1038/s41467-022-31773-8

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  2. Propagation of neuronal micronuclei regulates microglial characteristics

    Sarasa Yano, Natsu Asami, Yusuke Kishi, Ikuko Takeda, Hikari Kubotani, Yuki Hattori, Ayako Kitazawa, Kanehiro Hayashi, Ken-ichiro Kubo, Mai Saeki, Chihiro Maeda, Chihiro Hiraki, Rin-ichiro Teruya, Takumi Taketomi, Kaito Akiyama, Tomomi Okajima-Takahashi, Ban Sato, Hiroaki Wake, Yukiko Gotoh, Kazunori Nakajima, Takeshi Ichinohe, Takeshi Nagata, Tomoki Chiba, Fuminori Tsuruta

    Nature Neuroscience     2025.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1038/s41593-024-01863-5

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    Other Link: https://www.nature.com/articles/s41593-024-01863-5

  3. Neuromodulation with transcranial direct current stimulation contributes to motor function recovery via microglia in spinal cord injury. Reviewed International journal

    Ryotaro Oishi, Ikuko Takeda, Yukihito Ode, Yuya Okada, Daisuke Kato, Hiroaki Nakashima, Shiro Imagama, Hiroaki Wake

    Scientific reports   Vol. 14 ( 1 ) page: 18031 - 18031   2024.8

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    Language:English   Publishing type:Research paper (scientific journal)  

    Spinal cord injury (SCI) is damage or trauma to the spinal cord, which often results in loss of function, sensation, or mobility below the injury site. Transcranial direct current stimulation (tDCS) is a non-invasive and affordable brain stimulation technique used to modulate neuronal circuits, which changes the morphology and activity of microglia in the cerebral cortex. However, whether similar morphological changes can be observed in the spinal cord remains unclear. Therefore, we evaluated neuronal population activity in layer 5 (L5) of M1 following SCI and investigated whether changes in the activities of L5 neurons affect microglia-axon interactions using C57BL/6J mice. We discovered that L5 of the primary motor cortex (corticospinal neurons) exhibited reduced synchronized activity after SCI that correlates with microglial morphology, which was recovered using tDCS. This indicates that tDCS promotes changes in the morphological properties and recovery of microglia after SCI. Combining immunotherapy with tDCS may be effective in treating SCI.

    DOI: 10.1038/s41598-024-69127-7

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  4. A dopamine D1-like receptor-specific agonist improves the survival of septic mice. Reviewed International journal

    Koichi Tanaka, Mohammed E Choudhury, Satoshi Kikuchi, Ikuko Takeda, Kensuke Umakoshi, Noriyuki Miyaue, Kanta Mikami, Ayane Takenaga, Harumichi Yagi, Rintaro Shinabe, Hironori Matsumoto, Hajime Yano, Masahiro Nagai, Jun Takeba, Junya Tanaka

    iScience   Vol. 27 ( 4 ) page: 109587 - 109587   2024.4

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    In this study, a murine sepsis model was developed using the cecum ligation and puncture (CLP) technique. The expression of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) in the brain increased 6 h after CLP but decreased 24 h later when elevated endogenous dopamine levels in the brain were sustained. Methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride reduced dopamine levels in the striatum and increased mortality in septic mice. Dopamine D1-like receptors were significantly expressed in the brain, but not in the lungs. Intraperitoneally administered SKF-81297 (SKF), a blood-brain barrier-permeable D1-like receptor agonist, prevented CLP-induced death of septic mice with ameliorated acute lung injury and cognitive dysfunction and suppressed TNF-α and IL-1β expression. The D1-like receptor antagonist SCH-23390 abolished the anti-inflammatory effects of SKF. These data suggest that D1-like receptor-mediated signals in the brain prevent CLP-induced inflammation in both the brain and the periphery.

    DOI: 10.1016/j.isci.2024.109587

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  5. Activity-dependent oligodendrocyte calcium dynamics and their changes in Alzheimer's disease. Reviewed International journal

    Kenji Yoshida, Daisuke Kato, Shouta Sugio, Ikuko Takeda, Hiroaki Wake

    Frontiers in cellular neuroscience   Vol. 17   page: 1154196 - 1154196   2023.10

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    Language:English   Publishing type:Research paper (scientific journal)  

    Oligodendrocytes (OCs) form myelin around axons, which is dependent on neuronal activity. This activity-dependent myelination plays a crucial role in training and learning. Previous studies have suggested that neuronal activity regulates proliferation and differentiation of oligodendrocyte precursor cells (OPCs) and myelination. In addition, deficient activity-dependent myelination results in impaired motor learning. However, the functional response of OC responsible for neuronal activity and their pathological changes is not fully elucidated. In this research, we aimed to understand the activity-dependent OC responses and their different properties by observing OCs using in vivo two-photon microscopy. We clarified that the Ca2+ activity in OCs is neuronal activity dependent and differentially regulated by neurotransmitters such as glutamate or adenosine triphosphate (ATP). Furthermore, in 5-month-old mice models of Alzheimer's disease, a period before the appearance of behavioral abnormalities, the elevated Ca2+ responses in OCs are ATP dependent, suggesting that OCs receive ATP from damaged tissue. We anticipate that our research will help in determining the correct therapeutic strategy for neurodegenerative diseases beyond the synapse.

    DOI: 10.3389/fncel.2023.1154196

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Books 1

  1. 糖尿病診療ガイドライン

    竹田育子,大槻俊輔,松本昌泰( Role: Joint author ,  糖尿病における脳血管障害のリスク)

    南山堂  2011.2  ( ISBN:978-4-525-23821-6

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    Total pages:422  

MISC 17

  1. Psychiatric disorders and neuroinflammation: Approaching the multidirectional function of microglia

    竹田育子, 和氣弘明

    臨床精神医学   Vol. 53 ( 4 )   2024

  2. Holographic measurement and manipulation of multicellular circuit dynamics

    和氣弘明, 和氣弘明, 加藤大輔, 竹田育子, 竹田育子

    実験医学   Vol. 42 ( 7 )   2024

  3. 一次体性感覚野アストロサイトの活動制御による痛み関連行動の治療 Invited

    竹田育子

      Vol. 2   2023.4

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

  4. 【慢性疼痛】慢性疼痛とシナプス再編 グリア細胞制御による治療法を目指して

    鍋倉 淳一, 竹田 育子

    BRAIN and NERVE: 神経研究の進歩   Vol. 75 ( 3 ) page: 0207 - 0216   2023.3

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    Language:Japanese   Publisher:(株)医学書院  

    <文献概要>慢性疼痛は,痛覚過敏など体性感覚ばかりでなく,不安など多くの脳機能の異常を伴う。その病態メカニズムとして関連する脳部位の神経回路の長期変化が挙げられる。本論では,痛覚過敏を引き起こす病的回路構築へのグリア細胞の関与,および,異常感覚に関連する回路の可塑性を操作し,病的回路の修復と異常痛覚の除去の試みと臨床応用への期待について解説する。

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    Other Link: https://search.jamas.or.jp/default/link?pub_year=2023&ichushi_jid=J04871&link_issn=&doc_id=20230309260006&doc_link_id=10.11477%2Fmf.1416202310&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1416202310&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

  5. 体の「痛い」を脳から治す ―痛みに関わる神経回路を標的とした疼痛の新たな治療戦略― Invited

    竹田育子

    神経科学トピックス     2023.2

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

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Presentations 27

  1. 痛みに関わるニューロングリア連関から見た心・知・体ネットワーク Invited

    竹田育子

    女性研究者によるシンポジウム(APPW2025)  2025.3.16 

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    Event date: 2025.3

    Venue:幕張メッセ  

  2. The role of astrocyte in V2L neuronal remodeling following vision loss International conference

    Ikuko Takeda

    ASPIRE-GLIA Symposium  2024.9.17 

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    Event date: 2024.9

    Language:English   Presentation type:Oral presentation (general)  

    Country:Switzerland  

  3. アストロサイトの活動制御による慢性疼痛治療

    竹田育子

    第129回日本解剖学会総会・全国学術集会  2024.3.23 

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    Event date: 2024.3

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:沖縄   Country:Japan  

  4. 視覚喪失がもたらすアストロサイトによる高次視覚野V2Lの神経回路編成

    竹田 育子

    第10回 先進イメージング医学研究会  2024.3.1 

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    Event date: 2024.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:兵庫県  

  5. 色視覚入力による疼痛治療の開発

    竹田 育子

    JST-CREST「マルチセンシング」領域会議  2024.1.18 

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    Event date: 2024.1

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:京都 知恩院和順会館  

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Research Project for Joint Research, Competitive Funding, etc. 1

  1. 色から迫る慢性疼痛治療と神経回路基盤編成

    Grant number:2600007301  2022.4 - 2023.3

    堀科学芸術振興財団 研究費助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1000000

KAKENHI (Grants-in-Aid for Scientific Research) 6

  1. ミクログリアによる異種感覚の可塑性構築機序

    Grant number:21H05688  2021.9 - 2023.3

    科学研究費助成事業  学術変革領域研究(A)

    竹田 育子

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    Authorship:Principal investigator 

    Grant amount:\7800000 ( Direct Cost: \6000000 、 Indirect Cost:\1800000 )

  2. Cheromotherapy relieves pain by neural circuit organisation

    Grant number:23K06825  2023.4 - 2026.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

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  3. Development of pain treatment using color

    2023.4 - 2024.3

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  4. 感覚モダリティ理解のためのミクログリア・シナプス接触の多角的解析

    Grant number:20KK0170  2020.10 - 2024.3

    国際共同研究加速基金(国際共同研究強化(B))

    和氣 弘明

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    Authorship:Coinvestigator(s) 

    本国際研究では中枢神経系唯一の免疫細胞であるミクログリアに着目し、ミクログリアがシナプスの構造的・機能的可塑性を修飾する背景を踏まえ、多角的階層的な技術を相互補完することによって、ミクログリアのシナプスに対する時間的(発達・成熟)および空間(脳領域)特異的な生理機能を明らかにする。さらにこれを異種感覚の可塑的変化のメカニズムに繋げ、そこから精神病態を考察する。

  5. S1 astrocytes are therapeutic target for chronic pain

    Grant number:20K16510  2020.4 - 2022.3

    Grant-in-Aid for Early-Career Scientists

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    Authorship:Principal investigator 

    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

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Teaching Experience (On-campus) 15

  1. 肉眼解剖

    2024

  2. ベーシックトレーニングコース

    2024

  3. 基礎セミナーA

    2024

  4. 基礎医学体験実習

    2024

  5. 神経解剖

    2024

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