| Project/Area Number |
21790253
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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 |
General pharmacology
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| Research Institution | Hoshi University |
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Principal Investigator |
OHSAWA Masahiro Hoshi University, 薬学部, 講師 (80369173)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 糖尿病 / 痛覚過敏 / インスリン / グルタミン酸 / 神経科学 / 中枢神経系 / 薬理学 / グルタミン酸神経 / 視床外側核 / アロディニア / グルタミン酸神経系 / NMDA受容体 / AMPA受容体 / 有痛性神経障害 / 遺伝子発現 |
|---|
| Research Abstract |
Abnormal sensory perception in diabetes mellitus is very severe complications, which make patent life very inconvenient. The curative regimen for this complication does not established so far. The present study was investigate the novel mechanisms underlying in the diabetic sensory abnormal perception in the experimentally (streptozotocin-treated) induced diabetic mouse model. Intra-thalamic treatment with glutamate NMDA and AMPA receptor antagonist reduced the thermal and mechanical hypersensitivity in diabetic mice. This treatment did not affect the thermal and mechanical threshold in non-diabetic mice. Intra-thalamic treatment with glutamate, NMDA receptor agnonist and AMPA receptor agonist produced mechanical and thermal hypersensitivity in mice. Moreover, the expression of microglial marker Iba1 immunoreactivity was increased in diabetic mouse thalamus. These results suggested that abnormal sensory perception in diabetes mellitus may be due, in part, to the sensitization of pain pathway in the supraspianal site.
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