...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neurophysiology >Electrophysiological characteristics of reactive astrocytes in experimental cortical dysplasia.
【24h】

Electrophysiological characteristics of reactive astrocytes in experimental cortical dysplasia.

机译：实验性皮质发育不良中反应性星形胶质细胞的电生理特征。

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

Neocortical freeze lesions have been widely used to study neuronal mechanisms underlying hyperexcitability in dysplastic cortex. Comparatively little attention has been given to biophysical changes in the surrounding astrocytes that show profound morphological and biochemical alterations, often referred to as reactive gliosis. Astrocytes are thought to aid normal neuronal function by buffering extracellular K(+). Compromised astrocytic K(+) buffering has been proposed to contribute to neuronal dysfunction. Astrocytic K(+) buffering is mediated, partially, by the activity of inwardly rectifying K(+) channels (K(IR)) and may involve intracellular redistribution of K(+) through gap-junctions. We characterized K(+) channel expression and gap-junction coupling between astrocytes in freeze-lesion-induced dysplastic neocortex. Whole cell patch-clamp recordings were obtained from astrocytes in slices from postnatal day (P) 16--P24 rats that had received a freeze-lesion on P1. A marked increase in glial fibrillary acidic protein immunoreactivity was observed along the entire length of the freeze lesion. Clusters of proliferative (bromo-deoxyuridine nuclear staining, BrdU+) astrocytes were seen near the depth of the microsulcus. Astrocytes in cortical layer I surrounding the lesion were characterized by a significant reduction in K(IR). BrdU-positive astrocytes near the depth of the microsulcus showed essentially no expression of K(IR) channels but markedly enhanced expression of delayed rectifier K(+) (K(DR)) channels. These proliferative cells showed virtually no dye coupling, whereas astrocytes in the hyperexcitable zone adjacent to the microsulcus displayed prominent dye-coupling as well as large K(IR) and outward K(+) currents. These findings suggest that reactive gliosis is accompanied by a loss of K(IR) currents and reduced gap junction coupling, which in turn suggests a compromised K(+) buffering capacity.
机译：新皮层冷冻损伤已被广泛用于研究增生皮层中过度兴奋基础的神经元机制。对周围星形胶质细胞的生物物理变化的关注相对较少，这种变化显示出深刻的形态和生化改变，通常被称为反应性神经胶质增生。星形胶质细胞被认为可以通过缓冲细胞外K（+）来帮助正常的神经元功能。受损的星形细胞K（+）缓冲已被提议有助于神经元功能障碍。星形胶质K（+）缓冲部分地由向内整流K（+）通道（K（IR））的活动介导，并且可能涉及通过间隙连接的K（+）在细胞内的重新分布。我们表征了K（+）通道表达和星形胶质细胞在冷冻损伤诱导的增生性新皮层中的间隙连接耦合。全细胞膜片钳记录是从出生后（P）16-P24大鼠的切片中星形胶质细胞获得的，这些大鼠在P1上受到了冻伤。沿冷冻病变的整个长度观察到神经胶质纤维酸性蛋白免疫反应性显着增加。在微沟深处发现了星形胶质细胞增殖（溴脱氧尿苷核染色，BrdU +）。病变周围皮质层I中的星形胶质细胞的特征是K（IR）明显降低。微沟深度附近的BrdU阳性星形胶质细胞基本不显示K（IR）通道的表达，但显着增强了延迟整流K（+）（K（DR））通道的表达。这些增殖细胞几乎没有显示染料耦合，而邻近微沟的高兴奋区中的星形胶质细胞则显示出显着的染料耦合以及大的K（IR）和向外的K（+）电流。这些发现表明，反应性神经胶质增生伴随着K（IR）电流的损失和间隙连接耦合的减少，这反过来又暗示了K（+）缓冲能力的下降。

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