...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Dead-space microdomains hinder extracellular diffusion in rat neocortex during ischemia.
【24h】

Dead-space microdomains hinder extracellular diffusion in rat neocortex during ischemia.

机译：死区微域阻碍缺血过程中大鼠新皮层的细胞外扩散。

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

During ischemia, the transport of molecules in the extracellular space (ECS) is obstructed in comparison with healthy brain tissue, but the cause is unknown. Extracellular tortuosity (lambda), normally 1.6, increases to 1.9 in ischemic thick brain slices (1000 microm), but drops to 1.5 when 70,000 Mr dextran (dex70) is added to the tissue as a background macromolecule. We hypothesized that the ischemic increase in lambda arises from diffusion delays in newly formed dead-space microdomains of the ECS. Accordingly, lambda decreases when dead-space diffusion is eliminated by trapping dex70 in these microdomains. We tested our hypothesis by analyzing the diffusion of several molecules in neocortical slices. First we showed that diffusion of fluorescent dex70 in thick slices declined over time, indicating the entrapment of background macromolecules. Next, we measured diffusion of tetramethylammonium (TMA+) (74 Mr) to show that the reduction of lambda depended on the size of the background macromolecule. Thesynthetic polymer, 40,000 Mr polyvinylpyrrolidone, reduced lambda in thick slices, whereas 10,000 Mr dextran did not. The dex70 was also effective in normoxic slices (400 microm) after hypoosmotic stress altered the ECS to mimic ischemia. Finally, the dex70 effect was confirmed independently of TMA+ using fluorescent 3000 Mr dextran as a diffusion marker in thick slices: lambda decreased from 3.29 to 2.44. Taken together, these data support our hypothesis and offer a novel explanation for the origin of the large lambda observed in ischemic brain. A semiquantitative model of dead-space diffusion corroborates this new interpretation of lambda.
机译：在缺血期间，与健康的脑组织相比，分子在细胞外空间（ECS）中的运输受阻，但原因尚不清楚。在局部缺血的厚脑片（1000微米）中，细胞外弯曲（λ）通常为1.6，增加到1.9，但是当将70,000右旋糖酐（dex70）作为背景大分子添加到组织中时，其降低到1.5。我们假设lambda的缺血性增加是由于ECS新形成的死空间微区中的扩散延迟所致。因此，当通过在这些微区中捕获dex70消除死区扩散时，λ减小。我们通过分析新皮质切片中几个分子的扩散来检验我们的假设。首先，我们证明了荧光dex70在厚切片中的扩散随着时间的推移而下降，这表明背景大分子被捕获。接下来，我们测量了四甲基铵（TMA +）（74 Mr）的扩散，表明λ的减少取决于背景大分子的大小。合成聚合物40,000先生聚乙烯吡咯烷酮减少了厚片中的λ，而10,000先生右旋糖酐则没有。低渗应激改变ECS以模拟缺血后，dex70在常氧切片（400微米）中也有效。最后，使用荧光3000 Mr dextran作为扩散标记在厚切片中独立于TMA +证实了dex70的作用：λ从3.29降至2.44。综上所述，这些数据支持了我们的假设，并为缺血性脑中观察到的大λ的起源提供了新颖的解释。死空间扩散的半定量模型证实了这种对λ的新解释。

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