Transient hyperpolarization mechanism of the medial vestibular nucleus neurons to ischemia
Project/Area Number |
24791744
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Otorhinolaryngology
|
Research Institution | Gunma University |
Principal Investigator |
SHINO Masato 群馬大学, 医学部附属病院, 助教 (20550015)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 内側前庭神経核 / 虚血 / パッチクランプ / 発火特性 / スライスパッチクランプ / 内族前庭神経核 / 虚血耐性 / タイプAニューロン / タイプBニューロン |
Outline of Final Research Achievements |
We investigated electrophysiological response of MVN (Medial Vestibular Nucleus) neurons for transient ischemia. Transient ischemia induced transient hyperpolarization and pause of spontaneous firing. Transient hyperpolarization was attributed to intrinsic membrane property of MVN neurons. ATP sensitive potassium channel blocker, glibenclamide inhibited ischemia-induced transient hyperpolarization.
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Report
(4 results)
Research Products
(5 results)