| Project/Area Number |
24659827
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Functional basic dentistry
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Yoshinori 九州大学, 歯学研究院, 助教 (80582717)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 歯科薬理学 / Toll様受容体 / 神経障害性疼痛 / TOLL様受容体と慢性疼痛 / Unc93b / IFN- γ / ミクログリア |
|---|
| Research Abstract |
3d mice have defective signaling via TLR3, TLR7 and TLR9 due to the mutation of Unc93b1. In this study, the roles of these receptors on the induction of neuropathic pain were elucidated using 3d mice. 3d mice had statistically significant higher pain threshold as comparison with that of wild-type mice. In wild-type mice, the mean expression levels of inflammatory molecules in the spinal cord were significantly increased following peripheral nerve injury. In contrast, the mean expression levels of anti-inflammatory molecules were significantly increased in the spinal cord of 3d mice following peripheral nerve injury. These observations suggest that spinal microglia of wild-type mice polarize to M1 phenotype following peripheral nerve injury through activation of TLR9. On the other hand, spinal microglia in 3d mice polarize to M2 phenotype following peripheral nerve injury, inducing resistance to neuropathic pain.
|
