...
  • 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 >Respiratory survival mechanisms in acetylcholinesterase knockout mouse.
【24h】

Respiratory survival mechanisms in acetylcholinesterase knockout mouse.

机译：乙酰胆碱酯酶敲除小鼠的呼吸生存机制。

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

Cholinergic neurotransmission ensures muscle contraction and plays a role in the regulation of respiratory pattern in the brainstem. Inactivation of acetylcholinesterase (AChE) by organophosphates produces respiratory failure but AChE knockout mice survive to adulthood. Respiratory adaptation mechanisms which ensure survival of these mice were examined in vivo by whole body plethysmography and in vitro in the neonatal isolated brainstem preparation. AChE-/- mice presented no AChE activity but unaffected butyrylcholinesterase (BChE) activity. In vivo, bambuterol (50-500 microg/kg s.c.) decreased BChE activity peripherally but not in brain tissue and induced apnea and death in adult and neonate AChE-/- mice without affecting littermate AChE+/+ and +/- animals. In vitro, bath-applied bambuterol (1-100 microm) and tetraisopropylpyrophosphoramide (10-100 microm) decreased BChE activity in the brainstem but did not perturb central respiratory activity recorded from spinal nerve rootlets. In vitro, the cholinergic agonists muscarine (50-100 microm) and nicotine (0.5-10 microm) induced tonic activity in respiratory motoneurons and increased the frequency of inspiratory bursts in AChE+/+ and +/- animals. These effects were greatly attenuated in AChE-/- animals. The results suggest that, in mice lacking AChE, (i) BChE becomes essential for survival peripherally but plays no critical role in central rhythm-generating structures and (ii) a major adaptive mechanism for respiratory survival is the down-regulated response of central respiratory-related neurons and motoneurons to muscarinic and nicotinic agonists.
机译：胆碱能神经传递确保肌肉收缩并在脑干呼吸模式的调节中起作用。有机磷酸酯使乙酰胆碱酯酶（AChE）失活会导致呼吸衰竭，但敲除AChE的小鼠可以存活到成年。通过全身体积描记法在体内检查了确保这些小鼠存活的呼吸适应机制，并在新生儿分离的脑干制剂中进行了体外检查。 AChE-/-小鼠没有AChE活性，但未受影响的丁酰胆碱酯酶（BChE）活性。在体内，班布特罗（50-500微克/千克s.c.）外周降低BChE活性，但不在脑组织中降低，并在成年和新生AChE-/-小鼠中引起呼吸暂停和呼吸暂停和死亡，而不影响同窝AChE + / +和+/-动物。在体外，应用浴的班布特罗（1-100微米）和四异丙基焦磷酸酰胺（10-100微米）降低了脑干中的BChE活性，但并未扰乱脊神经根部记录的中枢呼吸活性。在体外，胆碱能激动剂毒蕈碱（50-100微米）和尼古丁（0.5-10微米）在呼吸运动神经元中诱导滋补活性，并增加了AChE + / +和+/-动物的吸气爆发频率。这些作用在AChE-/-动物中大大减弱。结果表明，在缺乏AChE的小鼠中，（i）BChE对周围存活至关重要，但在中枢节律产生结构中不发挥关键作用;（ii）呼吸存活的主要适应机制是中枢呼吸的下调反应毒蕈碱和烟碱样激动剂相关的神经元和运动神经元。

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