课题基金 / 基金详情

Role of glia cell during brain ischemia

Role of glia cell during brain ischemia
神经胶质细胞在脑缺血过程中的作用
批准号:
09680824
负责人:
YAMAMOTO Satoshi
金额:
$2.05万
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:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1999

项目摘要

项目成果

YAMAMOTO Satoshi的其他基金

相似基金

相关文献

中文摘要
翻译
点击翻译按钮获取中文摘要
英文摘要
Purpose : Analysis of Na,K-pump-induced currents in astrocytes and the role in brain ischemiaMethod : Using nystatin-perforated patch clamp techniques, Na,K-pump currents (Ip) were recorded from cultured astrocytes isolated from rat cerebral cortex.Results : 1. In the presence of intracellular Na([Na]I), Ip were activated by addition of extracellular K([K]o) in a dose-dependent manner with a Kd of O.8mM and a Hill coefficient of 1.7. 2.Ip were blocked by ouabain in a dose-dependent manner with a relatively high IC50 of about 0.1mM, suggesting the existence of a ouabain-resistant isoform in astrocytes. 3.Ip were increased in depolarized potentials and were decreased in hyperpolarized potential. Consequently, I-V relation of Ip showed a sigmoid shape. 4.Ip could be activated by [K]o even in the absence of [Na]I, suggesting the existence of non-inactivating Na currents that are not sensitive to tetrodotoxin. 5. In the presence of [Na]I, [K]o-induced Ip were augmented by removal of extracellular Na ([Na]o). 6. Metabolic inhibitor, sodium cyanide did not affect Ip function, suggesting that Ip activities are kept during brain ischemia. 7. Exogenous glutamate augmented Ip by increasing [Na]I. In some cases, the augmentation of Ip was evident after removal of glutamate, which is probably due to the phosphorylation of Na,K-ATPase via metabotropic-type glutamate receptors.Conclusion : From the all results, it is suggested that the Na,K-pump function in astrocytes is maintained during brain ischemia, and the activity is maximized by both elevation of [K]o and glutamate and reduction of [Na]o. These facts indicates that the Na,K-pump activity in astrocytes has a neuroprotective role in the removal of extracellular K accumulation during brain ischemia.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
Yamamoto, S., Higashi, H. 他: "Membrane dysfunction induced by in vitro ischemia in immature rat hippocampal CA1 neurons"Journal of Neurophysiology. 81. 1866-1871 (1999)
Yamamoto, S., Higashi, H. 等人:“未成熟大鼠海马 CA1 神经元体外缺血诱导的膜功能障碍”《神经生理学杂志》81. 1866-1871 (1999)。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Tanaka E., Yamamoto S., Inokuchi H., Isagai T., Higashi H.: "Membrane dysfunction induced by in vitro ischemia in rat hippocampal CA1 neurons."J. Neurophysiol. 81. 1866-1871 (1999)
Tanaka E.、Yamamoto S.、Inokuchi H.、Isagai T.、Higashi H.:“大鼠海马 CA1 神经元体外缺血诱导的膜功能障碍。”
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Yamamoto S., Tanaka E., Higashi H.: "Mediation by intracellular calcium-dependent signals of hypoxic hyperpolarization in rat hippocampal CA1 neurons in vitro."J. Neutophysiol. 77. 386-392 (1997)
Yamamoto S.、Tanaka E.、Higashi H.:“体外大鼠海马 CA1 神经元缺氧超极化的细胞内钙依赖性信号的介导。”J.
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Fujimura N., Tanaka E., Yamamoto S., Shigemori M., Higashi H.: "Contribution of ATP-sensitive potassium channels to hypoxic hypcrpolarization in rat hippocampal CA1 neurons in vitro."J. Neutophysiol. 77. 378-385 (1997)
Fujimura N.、Tanaka E.、Yamamoto S.、Shigemori M.、Higashi H.:“ATP 敏感钾通道对体外大鼠海马 CA1 神经元缺氧超极化的贡献”。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
18
    Chemical Composition of Disk Forming Regions of Solar-type Protostars and its Evolution to Planetary Systems
    • 批准号:
      18H05222
    • 项目类别:
      Grant-in-Aid for Scientific Research (S)
    • 资助金额:
      $120.22万
    • 财政年份:
      2018
    • 负责人:
      YAMAMOTO Satoshi
    • 依托单位:
    Study of a role of serotonin on a novel K channel in neuropathic pain.
    • 批准号:
      16K09004
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.0万
    • 财政年份:
      2016
    • 负责人:
      YAMAMOTO Satoshi
    • 依托单位:
    Study of a role of ATP on a novel K+ channel in neuropathic pain.
    • 批准号:
      25460731
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.33万
    • 财政年份:
      2013
    • 负责人:
      YAMAMOTO Satoshi
    • 依托单位:
    Study of a role of sympathetic nerves on a novel K+ channel in neuropathic pain.
    • 批准号:
      22600013
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.75万
    • 财政年份:
      2010
    • 负责人:
      YAMAMOTO Satoshi
    • 依托单位:
    国内基金
    海外基金
    Ascl1介导Wnt/beta-catenin通路在TLE海马硬化中反应性Astrocytes异常增生的作用及调控机制
    • 批准号:
      31760279
    • 项目类别:
      地区科学基金项目
    • 资助金额:
      35.0万元
    • 批准年份:
      2017
    • 负责人:
      丁银秀
    • 依托单位: