2010 Fiscal Year Final Research Report
Cellular mechanism of GluR2 about cell death in the spinal cord injury
| Project/Area Number |
20591746
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
YOSHIDA Munehito Wakayama Medical University, 医学部, 教授 (60201018)
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| Co-Investigator(Kenkyū-buntansha) |
NAKATSUKA Terumasa 関西医療大学, 保健医療学部, 教授 (30380752)
MIYAZAKI Nobuyuki 和歌山県立医科大学, 医学部, 助教 (90438276)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 脊髄損傷 / 神経科学 / 生理学 / シグナル伝達 / 細胞・組織 |
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| Research Abstract |
In this study, we investigated which was more vulnerable to ischemia, spinal ventral horn neurons or dorsal horn neurons by whole-cell patch-clamp methods with superfusingan oxygen- and glucose-deprived medium (ischemia simulating medium [ISM]). Ventral horn neurons are more vulnerable than dorsal horn neurons. Moreover, we clarified that hypothermia is neuroprotective against iscjemic insult in spinal ventral horn neurons. ISM exposure for several minutes generated an agonal inward current in VH neurons. This agonal inward current consisted of a slowand subsequent rapid inward current. In the presence of glutamate receptor antagonist, CNQX (10 μmol/L) and AP-5 (50 μmol/L), the average latency of the rapid inward currents in the VH neurons with ISM was significantly longer than the controls. However, the slope of the rapid inward current and the slope of the slow current in the presence of CNQX and AP-5 were not significantly smaller than that of the absence of these glutamate receptor antagonist.
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Research Products
(53 results)
