| Project/Area Number |
26460699
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Pain science
|
|---|
| Research Institution | Saga University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
八坂 敏一 佐賀大学, 医学部, 助教 (20568365)
吉田 裕樹 佐賀大学, 医学部, 教授 (40260715)
|
|---|
| Research Collaborator |
SASAGURI Tomoko
MURATA Yuzo
IIZASA Sayaka
ISHIKAWA Asako
HARA Hiromitsu
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | ＩＬ-27 / 痛覚過敏 / 感覚感度の調節 / 感覚過敏 / 痛みの調節 / IL-27 / ケラチノサイト |
|---|
| Outline of Final Research Achievements |
We show evidences that constitutive existence of IL-27 controls threshold of sensation that induce aversive behavior in physiological and pathological conditions. Mice lacking IL-27 signaling possessed chronic pain-like hypersensitivity without any treatments. Reconstitution of IL-27 in these mice reversed hypersensitive threshold of aversive behavior. Furthermore, these mice showed additional hypersensitivity when subjected to commonly used chronic pain models suggesting that the mechanism of hypersensitivity induced by ablation of IL-27 signaling was different from ones underlying known chronic pain models.
|
