• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Expert review of neurotherapeutics >Animal models for autosomal dominant frontal lobe epilepsy: on the origin of seizures.
【24h】

Animal models for autosomal dominant frontal lobe epilepsy: on the origin of seizures.

机译：常染色体显性遗传性额叶癫痫的动物模型：癫痫发作的起源。

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

Autosomal dominant frontal lobe epilepsy (ADNFLE) can be caused by mutations in either the alpha4 or beta2 subunit of the neuronal nicotinic Ach receptor. In vitro expression studies in Xenopus oocytes or human embryonic kidney cells have been proven to be valuable tools for the characterization of these mutations, but they do not fully resemble the situation in vivo. Compared with them, animal models have the advantage that the functional consequences of a given mutation can be studied in the complex context of an intact living organism. Recent transgenic and knock-in animal models and their valuable contributions to our current understanding of ADNFLE epileptogenesis are discussed in this article. Several of the mouse and rat models support the hypothesis that ADNFLE mutations cause seizures mainly by increasing GABAergic inhibition, and a conditional knock-in mouse model adds early embryonal structural changes as another possible pathogenetic mechanism.
机译：常染色体显性遗传性额叶癫痫（ADNFLE）可能是由神经元烟碱Ach受体的alpha4或beta2亚基突变引起的。已经证明在非洲爪蟾卵母细胞或人类胚胎肾细胞中进行体外表达研究是表征这些突变的有价值的工具，但它们与体内情况并不完全相似。与它们相比，动物模型的优势在于可以在完整的活生物体的复杂环境下研究给定突变的功能后果。本文讨论了最近的转基因和敲入动物模型及其对我们目前对ADNFLE癫痫发生的了解的宝贵贡献。几种小鼠和大鼠模型支持以下假设：ADNFLE突变主要通过增加GABA能抑制来引起癫痫发作，而条件性敲入小鼠模型增加了早期胚胎的结构变化，这是另一种可能的致病机制。

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