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Analysis of the communication-of-information system through glial cell in trigeminal ganglion

Research Project

Project/Area Number 22592270
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Surgical dentistry
Research InstitutionOsaka Dental University

Principal Investigator

TOKUNAGA Atsushi  大阪歯科大学, 歯学部, 講師(非常勤) (70254521)

Co-Investigator(Kenkyū-buntansha) KOTANI Junichiro  大阪歯科大学, 歯学部, 教授 (40109327)
SAKUMA Yasushi  大阪歯科大学, 歯学部, 准教授 (20205800)
Project Period (FY) 2010 – 2012
Project Status Completed (Fiscal Year 2012)
Budget Amount *help
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords三叉神経 / グリア / 情報システム / 三叉神経脊髄路核 / IL-18 / 下歯槽神経損傷モデル / 神経因性疼痛 / 行動試験 / ラット
Research Abstract

Interleukin -18 (IL-18) is an important regulator of innate and immune responses, and is known to be expressed in various types of cells and upregulated in pathological conditions including tissue injury and inflammation, suggesting it has both proinflammatory and compensatory roles. Here we show that IL-18 was increased in microglia in the trigeminal spinal subnucleus caudalis (Vc) after peripheral nerve injury. We used a trigeminal neuropathic pain model in which the withdrawal threshold of maxillary whisker pad skin was significantly decreased after inferior alveolar nerve transection, and observed a striking increase in IL-18 expression in the Vc around the obex area from3d and continued until 14d after nerve injury. The IL-18 labeled cells were largely colocalized with Iba1, suggesting this upregulation occurred in hyperactive microglia. We also found that the IL-18 induction coexisted with phosphorylated p38 MAPK, indicating a possible role of p38 in the regulation of IL-1.Our findings are the first report that injury of trigeminal nerve induced IL-18 upregulation in activated microglia in theVc, suggesting a possible role of IL-18 in orofacial neuropathic pain.

Report

(4 results)
  • 2012 Annual Research Report   Final Research Report ( PDF )
  • 2011 Annual Research Report
  • 2010 Annual Research Report
  • Research Products

    (2 results)

All 2010 Other

All Presentation (2 results)

  • [Presentation] 下歯槽神経損傷モデルにおける三叉神経脊髄路核でのIL-18の発現増加2010

    • Author(s)
      大郷英里奈、佐久間泰司、徳永敦、三好歓、野口光一、小谷順一郎
    • Organizer
      第109回近畿臨床歯科麻酔研究会大阪
    • Year and Date
      2010-03-29
    • Related Report
      2012 Final Research Report
  • [Presentation] 下歯槽神経損傷モデルにおける三叉神経脊髄路核でのIL-18の発現増加

    • Author(s)
      大郷英里奈
    • Organizer
      第109回近畿臨床歯科麻酔研究会
    • Place of Presentation
      大阪市
    • Related Report
      2012 Annual Research Report

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Published: 2010-11-30   Modified: 2019-07-29  

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