...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Glia >Ca2+ entry through TRPC1 channels contributes to intracellular Ca2+ dynamics and consequent glutamate release from rat astrocytes
【24h】

Ca2+ entry through TRPC1 channels contributes to intracellular Ca2+ dynamics and consequent glutamate release from rat astrocytes

机译：Ca2 +通过TRPC1通道进入有助于细胞内Ca2 +动力学，并因此从大鼠星形胶质细胞释放谷氨酸

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Astrocytes can respond to a variety of stimuli by elevating their cytoplasmic Ca2+ concentration and can in turn release glutamate to signal adjacent neurons. The majority of this Ca2+ is derived from internal stores while a portion also comes from outside of the cell. Astrocytes use Ca2+ entry through store-operated Ca2+ channels to refill their internal stores. Therefore, we investigated what role this store-operated Ca2+ entry plays in astrocytic Ca2+ responses and subsequent glutamate release. Astrocytes express canonical transient receptor potential (TRPC) channels that have been implicated in mediating store-operated Ca2+ entry. Here, we show that astrocytes in culture and freshly isolated astrocytes from visual cortex express TRPC1, TRPC4, and TRPC5. Indirect immunocytochemistry reveals that these proteins are present throughout the cell; the predominant expression of functionally tested TRPC1, however, is on the plasma membrane. Labeling in freshly isolated astrocytes reveals changes in TRPC expression throughout development. Using an antibody against TRPC1 we were able to block the function of TRPCI channels and determine their involvement in mechanically and agonist-evoked Ca2+ entry in cultured astrocytes. Blocking TRPC1 was also found to reduce mechanically induced Ca2+-dependent glutamate release. These data indicate that Ca2+ entry through TRPCI channels contributes to Ca2+ signaling in astrocytes and the consequent glutamate release from these cells. (C) 2008 Wiley-Liss, Inc.
机译：星形胶质细胞可以通过提高其胞质Ca2 +浓度来对多种刺激作出反应，并可以释放谷氨酸以向邻近的神经元发出信号。 Ca2 +的大部分来自内部存储，而一部分也来自细胞外部。星形胶质细胞通过存储操作的Ca2 +通道使用Ca2 +进入来补充其内部存储。因此，我们调查了这种存储操作的Ca2 +条目在星形细胞Ca2 +响应和随后的谷氨酸释放中起什么作用。星形胶质细胞表达规范的瞬时受体电位（TRPC）通道，这些通道与介导存储操作的Ca2 +进入有关。在这里，我们显示培养中的星形胶质细胞和来自视觉皮层的新鲜分离的星形胶质细胞表达TRPC1，TRPC4和TRPC5。间接免疫细胞化学揭示这些蛋白存在于整个细胞中。然而，功能测试的TRPC1的主要表达在质膜上。新鲜分离的星形胶质细胞中的标记揭示了整个发育过程中TRPC表达的变化。使用针对TRPC1的抗体，我们能够阻断TRPCI通道的功能，并确定它们参与培养的星形胶质细胞的机械和激动剂诱发的Ca2 +进入。还发现阻断TRPC1可减少机械诱导的Ca2 +依赖性谷氨酸释放。这些数据表明，通过TRPCI通道进入的Ca2 +有助于星形胶质细胞中的Ca2 +信号传导，并导致谷氨酸从这些细胞中释放出来。 （C）2008 Wiley-Liss，Inc.

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号