...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Glutamate transporter expression and function in a striatal neuronal model of Huntington's disease
【24h】

Glutamate transporter expression and function in a striatal neuronal model of Huntington's disease

机译：谷氨酸转运蛋白在亨廷顿氏病纹状体神经元模型中的表达和功能

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Excitotoxicity may contribute to the pathogenesis of Huntington's disease. High affinity Na+ dependent glutamate transporters, residing in the plasma membrane, clear glutamate from the extracellular space and are the primary means of protection against excitotoxicity. Many reports suggest that Huntington's disease is associated with a decrease in the expression and function of glutamate transporters. We studied the expression and function of these transporters in a cellular model of Huntington's disease, STHdh Q111/Q111 and STHdhQ7/Q7 cells. We found that only GLT-1b and EAAC1 were expressed in these cell lines and only EAAC1 significantly contributed to the glutamate uptake. Surprisingly, there was an increase in Na+-dependent glutamate uptake in STHdhQ111/Q111 cells accompanied by an increase in surface expression of EAAC1. We studied the influence of the Akt pathway on EAAC1 mediated uptake, since EAAC1 surface expression is influenced by Akt and previous studies have shown increased Akt expression in STHdhQ111/Q111 cells. Glutamate uptake was inhibited by Akt pathway inhibitors in both the STHdhQ7/Q7 and the STHdh Q111/Q111 cell lines. We found no difference in Akt activation between the two cell lines under our conditions of culture. Therefore a difference in Akt activation does not seem to explain the increase in EAAC1 mediated uptake in the STHdhQ111/Q111 cells.
机译：兴奋性毒性可能是亨廷顿舞蹈病的发病机理。高亲和力的Na +依赖性谷氨酸转运蛋白，位于质膜上，可从细胞外空间清除谷氨酸，是防止兴奋性毒性的主要手段。许多报告表明，亨廷顿舞蹈病与谷氨酸转运蛋白的表达和功能下降有关。我们研究了这些转运蛋白在亨廷顿氏病，STHdh Q111 / Q111和STHdhQ7 / Q7细胞模型中的表达和功能。我们发现，只有GLT-1b和EAAC1在这些细胞系中表达，并且只有EAAC1显着促进了谷氨酸的摄取。令人惊讶的是，伴随着EAAC1表面表达的增加，STHdhQ111 / Q111细胞中Na +依赖性谷氨酸的摄取增加。我们研究了Akt途径对EAAC1介导的摄取的影响，因为EAAC1表面表达受Akt影响，并且先前的研究表明STHdhQ111 / Q111细胞中Akt表达增加。在STHdhQ7 / Q7和STHdh Q111 / Q111细胞系中，Akt途径抑制剂均抑制谷氨酸的摄取。在我们的培养条件下，我们发现两种细胞系之间的Akt激活没有差异。因此，Akt激活的差异似乎不能解释EAAC1介导的STHdhQ111 / Q111细胞摄取的增加。

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