Project/Area Number |
26462331
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology
|
Research Institution | Niigata University |
Principal Investigator |
HONDA Hiroyuki 新潟大学, 医歯学総合病院, 講師 (20535174)
|
Co-Investigator(Kenkyū-buntansha) |
河野 達郎 東北医科薬科大学, 医学部, 教授 (00313536)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 麻酔薬 / 脊髄前角ニューロン / 神経保護 / 麻酔 / 脊髄前角運動ニューロン |
Outline of Final Research Achievements |
The elucidation of the immobilization mechanisms of the anesthetic agent in the spinal cord is important. However, the mechanisms in the ventral horn neurons is not clear. Furthermore, the protection mechanisms of the anesthetic agent for spinal cord ischemia is unknown. Therefore, in this study, we analyzed the mechanisms of the anesthetic agent in the ventral horn neurons. Nitrous oxide inhibited the glutamatergic excitatory postsynaptic currents in the ventral horn neurons. In contrast, the volatile anesthetics increased the gamma-aminobutyric acid mediated inhibitory postsynaptic currents. Furthermore, both of nitrous oxide and the volatile anesthetics extended the time before leading to cell death during the spinal cord ischemia. Thereby, we found that these anesthetic agents had ischemia-resistant effects in ventral horn neurons.
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