• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Nature >Hippocampal GABA transporter function in temporal-lobe epilepsy.
【24h】

Hippocampal GABA transporter function in temporal-lobe epilepsy.

机译：海马GABA转运蛋白在颞叶癫痫中的作用。

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

Electrophysiological studies of human temporal-lobe epilepsy suggest that a loss of hippocampal GABA-mediated inhibition may underlie the neuronal hyperexcitability. However, GABA (gamma-aminobutyric acid)-containing cells are preserved and GABA receptors are maintained in the surviving hippocampal neurons. Diminished GABA release may therefore mediate the loss of inhibition. Here we show that, in the human brain, potassium-stimulated release of GABA was increased, and glutamate-induced, calcium-independent release of GABA was markedly decreased, in epileptogenic hippocampi, in contrast with contralateral, non-epileptogenic hippocampi. The glutamate-induced GABA release in vivo was transporter-mediated in rats. Furthermore, in amygdala-kindled rats, a model for human epilepsy, a decrease in glutamate-induced GABA release was associated with a 48% decrease in the number of GABA transporters. These data suggest that temporal-lobe epilepsy is characterized in part by a loss of glutamate-stimulated GABA release that is secondary to a reduction in the number of GABA transporters.
机译：人类颞叶癫痫的电生理研究表明，海马GABA介导的抑制作用的丧失可能是神经元过度兴奋的基础。但是，在存活的海马神经元中保留了含有GABA（γ-氨基丁酸）的细胞，并保留了GABA受体。因此，GABA释放减少可能会介导抑制作用的丧失。在这里，我们显示，与对侧，非癫痫性海马相比，在癫痫性海马中，钾刺激的GABA释放增加，而谷氨酸诱导的钙非依赖性GABA释放明显减少。大鼠体内谷氨酸诱导的GABA释放是转运蛋白介导的。此外，在杏仁核型大鼠（一种用于人类癫痫的模型）中，谷氨酸诱导的GABA释放减少与GABA转运蛋白数目减少48％有关。这些数据表明颞叶癫痫的特征部分在于谷氨酸刺激的GABA释放的丧失，这是继GABA转运蛋白数量减少之后的结果。

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