Cyte-physiological study of abnormal Ca^<2+> metabolism in delayed neuronal death
| Project/Area Number |
15591543
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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 |
Cerebral neurosurgery
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| Research Institution | Jichi Medical School |
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Principal Investigator |
OGURO Keiji Jichi Medical School, Surgical Neurology, Assistant professor, 医学部, 講師 (90231232)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMAZAKI Kuniko Jichi Medical School, Physiology, Assistant professor, 医学部, 講師 (40142153)
WATANABE Eiju Jichi Medical School, Surgical Neurology, Professor, 医学部, 教授 (50150272)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cerebral ischemia / calcium / hippocampus / resistance / slice / GluR2 / IP_4 |
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| Research Abstract |
Ischemic resistance of developing gerbils
To investigate the mechanisms by which developing animals exhibit ischemic resistance, we examined the changes in intracellular calcium ([Ca^<2+>]i) after oxygen-glucose deprivation (OGD) using hippocampal slices form gerbils. We found that increases in [Ca^<2+>]i in hippocampal CA1 neurons is significantly less after OGD in developing gerbils than in adults. We then examined the expression of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors (AMPARs) GluR1-4 during the developmental period by Western blot analysis. We also investigated the anti-apoptotic proteins HSP70,Bcl-XL and plasma membrane Ca^<2+>-ATPase type 1 (PMCA1). GluR2 expression, but not that of the other AMPARs, is significantly higher in developing gerbils than in adults. These results suggest that the higher expression of GluR2 is important for the smaller increases in [Ca^<2+>]i and enhanced resistance to ischemia-induced neuronal damage in developing anim
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Functional changes in IP_33 kinase knock-out mice
IP_33-kinase metabolizes IP_3 to 1,3,4,5-tetrakisphosphate (IP_4). Until recently physiological roles of IP_33-kinase or IP_4 are not well known. IP_33-kinase (A) is abundant in neuronal cells and IP_4 level in IP_33-kinase(A) deficient mice is significantly decreased. To know the role of IP_33-kinase or IP_4 in neuronal tissue, histochemical, behavioral and physiological study were performed using IP_33-kinase(A) deficient and wild type mice. In histochemical study with IP_33-kinase antibody, IP_33-kinase strongly express in hioppocampal CA1 region in normal gerbil. Passive avoidance with electric shocking chamber revealed less learning and memory function in IP_33-kinase(A) deficient mice. Hippocampal damage induced by global ischemia by 10 min common carotid occlusion did not show significant differences between IP_33-kinase(A) deficient and wild type mice. Intracellular Ca^<2+> increase following oxygen-glucose deprivation was also examined using hippocampal slice of deficient and wild type mice. These results suggest that IP_33-kinase and IP_4 have important roles in the process of learning and memory. Less
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Report
(3 results)
Research Products
(12 results)
