| Project/Area Number |
21700400
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | University of Toyama |
|---|
Principal Investigator |
TAKASAKI Ichiro 富山大学, 生命科学先端研究センター, 助教 (00397176)
|
|---|
| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 帯状疱疹痛 / 帯状疱疹後神経痛 / IE62 / 帯状疱疹 / 脳由来神経栄養因子 / アロディニア / Galectin-3 / 帯状庖疹 / 帯状庖疹後神経痛 |
|---|
| Research Abstract |
Acute herpetic pain and postherpetic neuralgia are intractable neurogenic pain, however the mechanisms of the pain are still unknown. We previously found that immunoreaction to antibody to IE62, one of immediate early protein produced by varicella zoster virus, augment mechanical allodynia in mice with peripheral nerve injury via activation of BDNF activity. In this research, we found that antibody to IE62 augment the acute herpetic pain and increase the transition to postherpetic neuralgia in mice. Using global gene expression analysis, we revealed that spinal galectin-3 is involved in the acute herpetic allodynia. However, we found that galectin-3 is not involved in the anti-IE62 antibody-mediated augmentation of mechanical allodynia.
|
