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Cyte-physiological study of abnormal Ca^<2+> metabolism in ischemic and epileptic neuronal death

Cyte-physiological study of abnormal Ca^<2+> metabolism in ischemic and epileptic neuronal death
缺血性和癫痫性神经元死亡中异常 Ca^<2> 代谢的细胞生理学研究
批准号:
17591527
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:
2005
资助国家:
日本
项目状态:
已结题
起止时间:
2005 至 2006

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中文摘要
翻译
IP_33K基因敲除小鼠IP_33-激动素代谢IP_3为1,3,4,5-四磷酸(IP_4)的功能变化。直到最近,对IP_33-激酶或IP_4的生理作用还不是很清楚。IP_33-K(A)在神经细胞中含量丰富,IP_4水平在IP_33-K(A)缺乏的小鼠中显著降低。为了解IP_33-K(A)或IP_4在神经元组织中的作用,对IP_33-K(A)缺陷小鼠和野生型小鼠进行了组织化学、行为学和生理学研究。在IP_33-K抗体的组织化学研究中,IP_33-K在正常沙土鼠海马区CA1区有较强的表达。电击室被动回避显示IP_33-K(A)缺陷小鼠的学习记忆功能下降。IP_33-K(A)缺陷型和野生型小鼠在颈总动脉结扎10min造成的全脑缺血所致的海马区损伤无明显差异。缺氧缺糖后细胞内Ca~(2+)升高也可检测到…更多地使用缺陷和野生型小鼠的海马片。这些结果表明,IP_33-激酶和IP_4在学习记忆过程中起着重要作用。增强EL小鼠海马神经元的兴奋性。我们用Rhod2-AM钙成像技术观察了缺氧缺糖(OGD)后EL和对照DDY小鼠海马片上细胞内钙的变化。EL小鼠OGD后海马区CA1、CA3区细胞内钙离子显著升高。而对照组DDY小鼠仅在CA1区有表达增加。我们还在发育中的动物(2-8周)中进行了同样的实验,以了解何时可以看到CA3的超兴奋性。在发育中的EL小鼠中,在CA1和CA3中,OGD后钙的增加平均小于成年鼠。随着年龄的增加,CA1和CA3的荧光强度依次增强。这些结果表明,EL小鼠海马CA3区兴奋性增强是随着年龄的增长而逐渐增强的。这不是增长后的收购。较少
英文摘要
Functional changes in IP_33kinase knock-out miceIP_33-kinasemetabolizu 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 exam … More ined 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.Enhanced excitability on hippocampal CA3 in EL miceWe observed the changes in intracellular calcium on EL and control DDY mice hippocampal slice after oxygen-glucose deprivation (OGD) using calcium imaging with Rhod2-AM. In EL mice, the cytosolic calcium on hippocampal CA1, CA3 was significantly increased after OGD. On the contrary control DDY mice showed increase just on CA1 region. We also performed the same experiments in developing animals (2-8w) to know from when the hyper excitability in CA3 can be seen. In developing EL mice, calcium increase after OGD was less than the adults evenly in CA1 and CA3. The fluorescent intensity was successively increased in both CA1 and CA3 according to its age. These results suggest that the enhanced excitability on hippocampal CA3 in EL mice is obtained gradually according to the age. It is not a postgrowth acquisition. Less
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イオンチャネルを共有する受容体.グルタミン酸.In:生物薬科学実験講座- 情報伝達物質 [I]受容体-(石橋貞彦, 市川厚, 堅田利明 編)
共享离子通道的受体。谷氨酸.In:生物制药科学实验课程 - 信息传送器 [I] 受体 -(石桥贞彦、市川敦、方俊明编辑)
DOI: --
发表时间: 2005
期刊:
影响因子: --
作者: [島崎久仁子, 川合述史]
通讯作者: 川合述史
てんかん外科の術前診断の現状
癫痫手术术前诊断现状
DOI: --
发表时间: 2007
期刊: 脳神経外科ジャーナル 16
影响因子: --
作者: [横田英典, 小黒恵司, 渡辺英寿]
通讯作者: 渡辺英寿
Zine-dependent multi-conductance channel activity in mitochondria Isolated from ischemic brain.
从缺血脑中分离的线粒体中锌依赖性多电导通道活性。
DOI: --
发表时间: 2006
期刊: J Neurosci 26
影响因子: --
作者: [Bonanni L, Yokota H, Sensi SL, Zukin RS, Jonas EA, et al.]
通讯作者: et al.
Differential effects of sublethal ischemia and chemical preconditioning with 3-nitropropionic acid on protein expression in gerbil hippocampus.
亚致死缺血和 3-硝基丙酸化学预处理对沙鼠海马蛋白表达的差异影响。
DOI: --
发表时间: 2005
期刊: Life Sciences 77
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
共 14 条
    Cyto-physiological study of abnormal Ca^<2+> metabolism in ischemic and epileptic neuronal death
    • 批准号:
      19591699
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.91万
    • 财政年份:
      2007
    • 负责人:
      OGURO Keiji
    • 依托单位:
    Cyte-physiological study of abnormal Ca^<2+> metabolism in delayed neuronal death
    • 批准号:
      15591543
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.24万
    • 财政年份:
      2003
    • 负责人:
      OGURO Keiji
    • 依托单位:
    Cell biological study of glutamate receptor and gap jujunction in delyed neuronal death
    • 批准号:
      11671383
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.3万
    • 财政年份:
      1999
    • 负责人:
      OGURO Keiji
    • 依托单位:
    Histochemical and physiological study of delayd neuronal death
    • 批准号:
      08671608
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $0.45万
    • 财政年份:
      1996
    • 负责人:
      OGURO Keiji
    • 依托单位:
    国内基金
    海外基金
    Calcium/NFAT/GLUT3通路调控糖酵解代谢在CAR-T细胞耗竭中的作用和机制研究
    • 批准号:
      --
    • 项目类别:
      面上项目
    • 资助金额:
      52万元
    • 批准年份:
      2022
    • 负责人:
      张明明
    • 依托单位:
    钙信号负向调节因子IRBIT抑制肝癌细胞恶性生物学行为的分子机制研究
    • 批准号:
      31960151
    • 项目类别:
      地区科学基金项目
    • 资助金额:
      40.0万元
    • 批准年份:
      2019
    • 负责人:
      徐靖宇
    • 依托单位:
    基于钙信号特征机制的肿瘤转移调控研究
    • 批准号:
      31970729
    • 项目类别:
      面上项目
    • 资助金额:
      58.0万元
    • 批准年份:
      2019
    • 负责人:
      魏朝亮
    • 依托单位:
    一种拟南芥IP3结合蛋白作用机制及功能研究
    • 批准号:
      31970723
    • 项目类别:
      面上项目
    • 资助金额:
      60.0万元
    • 批准年份:
      2019
    • 负责人:
      韩生成
    • 依托单位: