...
  • 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 >Orexin gene transfer into the amygdala suppresses both spontaneous and emotion-induced cataplexy in orexin-knockout mice
【24h】

Orexin gene transfer into the amygdala suppresses both spontaneous and emotion-induced cataplexy in orexin-knockout mice

机译：食欲素基因转移到杏仁核中抑制食欲素基因敲除小鼠的自发性和情绪诱发的瘫痪

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

Narcolepsy is a chronic sleep disorder linked to the loss of orexin-producing neurons in the hypothalamus. Cataplexy, a sudden loss of muscle tone during waking, is an important distinguishing symptom of narcolepsy and it is often triggered by strong emotions. The neural circuit underlying cataplexy attacks is not known, but is likely to involve the amygdala, a region implicated in regulating emotions. In mice models of narcolepsy, transfer of the orexin gene into surrogate neurons has been successful in ameliorating narcoleptic symptoms. However, it is not known whether this method also blocks cataplexy triggered by strong emotions. To examine this possibility, the gene encoding mouse prepro-orexin was transferred into amygdala neurons of orexin-knockout (KO) mice (rAAV-orexin; n=8). Orexin-KO mice that did not receive gene transfer (no-rAAV; n=7) or received only the reporter gene (rAAV-GFP; n=7) served as controls. Three weeks later, the animal's sleep and behaviour were recorded at night (no-odour control night), followed by another recording at night in the presence of predator odour (odour night). Orexin-KO mice given the orexin gene transfer into surrogate amygdala neurons had significantly less spontaneous bouts of cataplexy, and predator odour did not induce cataplexy compared with control mice. Moreover, the mice with orexin gene transfer were awake more during the odour night. These results demonstrate that orexin gene transfer into amygdala neurons can suppress both spontaneous and emotion-induced cataplexy attacks in narcoleptic mice. It suggests that manipulating amygdala pathways is a potential strategy for treating cataplexy in narcolepsy.
机译：发作性睡病是一种慢性睡眠障碍，与下丘脑中产生食欲素的神经元丢失有关。 Cataplexy，醒来时突然失去肌肉张力，是发作性睡病的重要区别症状，通常由强烈的情绪触发。瘫痪发作的神经回路尚不清楚，但可能涉及杏仁核，杏仁核是调节情绪的区域。在发作性睡病的小鼠模型中，将orexin基因转移到替代性神经元中已成功缓解了发作性发作症状。然而，尚不知道这种方法是否也能阻止强烈情绪触发的昏厥。为了检验这种可能性，将编码小鼠前原胃泌素的基因转移到了orexin敲除（KO）小鼠的杏仁核神经元中（rAAV-orexin; n = 8）。不接受基因转移（no-rAAV; n = 7）或仅接受报告基因（rAAV-GFP; n = 7）的Orexin-KO小鼠作为对照。三个星期后，在夜间（无气味的夜晚）记录了动物的睡眠和行为，随后在有捕食者气味的夜间（气味夜晚）记录了动物的睡眠和行为。将Orexin基因转移到替代的杏仁核神经元中的Orexin-KO小鼠与对照小鼠相比，自发性的瘫痪发作明显减少，并且捕食者的气味不会引起瘫痪。此外，在有异味的夜晚，具有orexin基因转移的小鼠更加清醒。这些结果表明食欲素基因转移到杏仁核神经元可以抑制自感和情绪诱发的发作性发作的发作性发作小鼠中。这表明操纵杏仁核途径是治疗发作性睡病中瘫痪的一种潜在策略。

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