| Project/Area Number |
26861381
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Otorhinolaryngology
|
|---|
| Research Institution | Kobe University |
|---|
Principal Investigator |
INOKUCHI GO 神戸大学, 医学(系)研究科(研究院), 助教 (10457046)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | オリーブ蝸牛束 / Reelin / Dab1 / 聴力障害 / リーリン / 難聴 / 音響外傷 / 加齢性難聴 |
|---|
| Outline of Final Research Achievements |
MMedial olivocochlear neurons (MOC) originate in the superior olivary complex and project to the cochlea. MOC neurons have a role in acoustic efferent feedback, which suppresses the cochlear amplification of outer hair cells.
In the present study, we use the different Dab1-deficient mice (yotari) and investigate the position of MOC neurons in ventral nucleus of trapezoid body (VNTB). Immunohistochemistry revealed that MOC neurons were absent in VNTB and scattered around the motor vestibular nucleus. Auditory brainstem response (ABR) showed the elevated threshold of hearing only in mutated mice.
Thus, Dab-1 mutated mice are lack of MOC feedback, which has a protective effect of cochlea against surrounding noise. Dab-1 mutated mice could be the model of accelerated age-related hearing loss due to MOC feedback.
|
