Cyte-physiological study of abnormal Ca^<2+> metabolism in delayed neuronal death
Cyte-physiological study of abnormal Ca^<2+> metabolism in delayed neuronal death
批准号:
15591543
负责人:
OGURO Keiji
金额:
$2.24万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004
中文摘要
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英文摘要
Ischemic resistance of developing gerbilsTo 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 … More als.Functional changes in IP_33 kinase knock-out miceIP_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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虚血性神経細胞死とギャップ結合in脳血管障害による「神経細胞死」の予防と治療(川合述史編)
脑血管疾病引起的缺血性神经元死亡和“神经元死亡”中间隙连接的预防和治疗(河合正史编辑)
DOI:
--
发表时间:
2003
期刊:
影响因子:
--
作者:
[小黒恵司, 田中秀信, 横田英典, 宮脇貴裕]
通讯作者:
宮脇貴裕
Oguro K, Miyawaki T, Yokota H, Kato, M, Watanabe M, Shimazaki K, et al.: "Upregulation of GluR2 decreases intracellular Ca^<2+> following ischemia in developing gerbils"Neurosci.Letter. (in press). (2004)
Oguro K、Miyawaki T、Yokota H、Kato, M、Watanabe M、Shimazaki K 等人:“GluR2 的上调可减少发育中沙鼠缺血后的细胞内 Ca^2””Neurosci.Letter。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Ischemic neuronal death and gap junctions.
缺血性神经元死亡和间隙连接。
DOI:
--
发表时间:
2003
期刊:
Prevention and therapy for neuronal death by cerebrovascular disease (Kawai N ed.) Tokyo
影响因子:
--
作者:
[Oguro K, Tanaka H, Yokota H, Miyawaki T.]
通讯作者:
Miyawaki T.
Ischemic tolerance with 3-nitropionic acid induces the over expression of Bcl-2 and Bcl-_<XL> but lacking for HSP70 and plasma membrane Ca^<2+>-ATPase type 1.
3-硝基丙酸的缺血耐受诱导 Bcl-2 和 Bcl-_<XL> 过度表达,但缺乏 HSP70 和质膜 Ca^2-ATPase 1 型。
DOI:
--
发表时间:
2005
期刊:
Life Science (in press)
影响因子:
--
作者:
[Kato K, Shimazaki K, Kamiya T, Amemiya S, Inaba T, Oguro K, Katayama Y.]
通讯作者:
Katayama Y.
Upregulation of GluR2 decreases intracellular Ca2+ following ischemia in developing gerbils.
发育中的沙鼠缺血后,GluR2 的上调会减少细胞内 Ca2+。
DOI:
--
发表时间:
2004
期刊:
Neurosci Letters 364
影响因子:
--
作者:
[Oguro K, Miyawaki T, Hokota H, Kato K, Kamiya T, Katayama Y, Fukaya M, Watanabe M, Shimazaki K.]
通讯作者:
Shimazaki K.
共 11 条
Cyto-physiological study of abnormal Ca^<2+> metabolism in ischemic and epileptic neuronal death
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批准号:19591699
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.91万
-
财政年份:2007
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负责人:OGURO Keiji
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依托单位:
Cyte-physiological study of abnormal Ca^<2+> metabolism in ischemic and epileptic neuronal death
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批准号:17591527
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.24万
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财政年份:2005
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负责人:OGURO Keiji
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依托单位:
Cell biological study of glutamate receptor and gap jujunction in delyed neuronal death
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批准号:11671383
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.3万
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财政年份:1999
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负责人:OGURO Keiji
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依托单位:
Histochemical and physiological study of delayd neuronal death
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批准号:08671608
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$0.45万
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财政年份:1996
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负责人:OGURO Keiji
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依托单位:
国内基金
海外基金
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