...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neurophysiology >GABA receptor inhibition and severe hypoxia induce a paroxysmal depolarization shift in goldfish neurons.
【24h】

GABA receptor inhibition and severe hypoxia induce a paroxysmal depolarization shift in goldfish neurons.

机译：GABA受体抑制和严重缺氧诱导金鱼神经元中的阵发性去极化移位。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Mammalian neurons undergo rapid excitotoxic cell death when deprived of oxygen; however, the common goldfish ( Carassius auratus ) has the unique ability of surviving in oxygen-free waters, under anoxia. This organism utilizes γ-amino butyric acid (GABA) signaling to suppress excitatory glutamatergic activity during anoxic periods. Although GABA_(A)receptor antagonists are not deleterious to the cellular survival, coinhibition of GABA_(A)and GABA_(B)receptors is detrimental by abolishing anoxia-induced neuroprotective mechanisms. Here we show that blocking the anoxic GABAergic neurotransmission induces seizure-like activity (SLA) analogous to a paroxysmal depolarization shift (PDS), with hyperpolarization of action potential (AP) threshold and elevation of threshold currents. The observed PDS was attributed to an increase in excitatory postsynaptic currents (EPSCs) that are normally attenuated with decreasing oxygen levels. Furthermore, for the first time, we show that in addition to PDS, some neurons undergo depolarization block and do not generate AP despite a suprathreshold membrane potential. In conclusion, our results indicate that with severe hypoxia and absence of GABA receptor activity, telencephalic neurons of C. auratus manifest a paroxysmal depolarization shift, a key feature of epileptic discharge. NEW & NOTEWORTHY This work shows that the combination of anoxia and inhibition of GABA receptors induces seizure-like activities in goldfish telencephalic pyramidal and stellate neurons. Importantly, to prevent seizure-like activity, an intact GABA-mediated inhibitory pathway is required.
机译：哺乳动物神经元在缺氧时会经历快速的兴奋性毒性细胞死亡；然而，普通金鱼（Carassius auratus）具有在缺氧条件下在无氧水域生存的独特能力。这种生物体利用γ-氨基丁酸（GABA）信号来抑制缺氧期间的兴奋性谷氨酸能活动。尽管GABA_（A）受体拮抗剂对细胞存活没有损害，但通过消除缺氧诱导的神经保护机制，GABA_（A）和GABA_（B）受体的共同抑制是有害的。在这里，我们表明，阻断缺氧GABA能神经传递可诱导类似于阵发性去极化移位（PDS）的癫痫样活动（SLA），伴随着动作电位（AP）阈值的超极化和阈值电流的升高。观察到的PDS归因于兴奋性突触后电流（EPSC）的增加，这些电流通常随着氧气水平的降低而减弱。此外，我们首次表明，除了PDS，一些神经元经历去极化阻滞，尽管存在阈上膜电位，但不产生AP。总之，我们的结果表明，在严重缺氧和缺乏GABA受体活性的情况下，金鲫的端脑神经元表现出阵发性去极化移位，这是癫痫放电的一个关键特征。新的和值得注意的这项研究表明，缺氧和GABA受体抑制的结合在金鱼端脑锥体和星状神经元中诱导癫痫样活动。重要的是，为了防止癫痫样活动，需要一个完整的GABA介导的抑制途径。

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