2012 Fiscal Year Final Research Report
Analysis of the communication-of-information system through glial cell in trigeminal ganglion
| Project/Area Number |
22592270
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Osaka Dental University |
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Principal Investigator |
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| 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)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 三叉神経 / グリア / 情報システム |
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| 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.
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