| Project/Area Number |
19791554
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
OKUMURA Masayo Matsumoto Dental University, 総合歯科医学研究所, 助教 (10362849)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,170,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥570,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | 神経損傷 / 遺伝子発現 / Gabapentin / CACNA2D1 / 神経 / 疼痛 / モデルラット / 臨床例 |
|---|
| Research Abstract |
I detected up-regulations of many gene expressions in trigeminal ganglion of inferior alveolar nerve (IAN) transaction model rat, one of many neuropathic pain model. The allodynia was inhibited by an anticonvulsant, gabapentin, which was infused to medullary through an indwelling catheter. Although many genes were up-regulated in the trigeminal ganglion of the IAN transacted rats, only the up-regulated expression of CACNA2D1, a subunit of voltage-dependent calcium channel, was reversed by gabapentin, along with inhibition of allodynia.
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