...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Selective sparing of hippocampal CA3 cells following in vitro ischemia is due to selective inhibition by acidosis.
【24h】

Selective sparing of hippocampal CA3 cells following in vitro ischemia is due to selective inhibition by acidosis.

机译：体外缺血后海马CA3细胞的选择性保留是由于酸中毒引起的选择性抑制。

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

A brief global ischemic insult to the brain leads to a selective degeneration of the pyramidal neurons in the hippocampal CA1 region while the neurons in the neighbouring CA3 region are spared. The reason for this difference is not known. The selective vulnerability of CA1 neurons to ischemia can be reproduced in vitro in murine organotypic slice cultures, if the ion concentrations in the medium during the anoxic/aglycemic insult are similar to that in the brain extracellular fluid during ischemia in vivo. As acidosis develops during ischemia, we studied the importance of extracellular pH for selective vulnerability. We found that cell death in the CA1 and CA3 regions was equally prevented by removal of calcium from the medium or following blockade of the N-methyl-d-aspartate (NMDA) receptor by d-2 amino-5-phosphonopentanoic-acid (D-APV). On the other hand, damage to the CA3 neurons markedly decreased with decreasing pH following in vitro ischemia, while the degeneration of CA1 neurons was less pH dependent. Patch-clamp recordings from pyramidal neurons in the CA1 and CA3 regions, respectively, revealed a pronounced inhibition of NMDA-receptor mediated excitatory postsynaptic currents (EPSCs) at pH 6.5 that was equally pronounced in the two regions. However, when changing pH from 6.5 to 7.4 the recovery of the EPSCs was significantly slower in the CA3 region. We conclude that acidosis selectively protects CA3 pyramidal neurons during in vitro ischemia, and differentially affects the kinetics of NMDA receptor activation, which may explain the difference in vulnerability between CA1 and CA3 pyramidal neurons to an ischemic insult.
机译：对大脑的短暂性全局缺血性损伤会导致海马CA1区锥体神经元选择性变性，而邻近CA3区的神经元则被保留。这种差异的原因尚不清楚。如果缺氧/无糖血症损伤期间培养基中的离子浓度与体内缺血期间脑细胞外液中的离子浓度相似，则可以在鼠类器官切片培养物中体外复制CA1神经元对局部缺血的选择性脆弱性。随着缺血期间酸中毒的发展，我们研究了细胞外pH对选择性脆弱性的重要性。我们发现，通过从培养基中去除钙或在D-2氨基-5-膦基戊酸（D-）阻断N-甲基-d-天冬氨酸（NMDA）受体后，同样可以防止CA1和CA3区的细胞死亡。 -APV）。另一方面，在体外缺血后，随着pH降低，对CA3神经元的损害明显减少，而CA1神经元的变性则对pH依赖性较小。分别在CA1和CA3区的锥体神经元的膜片钳记录表明，在pH 6.5时，NMDA受体介导的兴奋性突触后电流（EPSC）受到了明显抑制，在这两个区域中同样明显。但是，将pH从6.5更改为7.4时，CA3区域中EPSC的回收明显降低。我们得出的结论是，酸中毒在体外缺血期间选择性保护了CA3锥体神经元，并差异性地影响NMDA受体激活的动力学，这可能解释了CA1和CA3锥体神经元对缺血性损伤的脆弱性差异。

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