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首页> 外文学位 >GABA Receptor and KCa Channel-mediated Electrical Suppression in Anoxic Cortical Pyramidal Neurons of the Painted Turtle (Chrysemys picta bellii).
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GABA Receptor and KCa Channel-mediated Electrical Suppression in Anoxic Cortical Pyramidal Neurons of the Painted Turtle (Chrysemys picta bellii).

机译：GABA受体和KCa通道介导的彩龟缺氧皮层锥体神经元的电抑制（Chrysemys picta bellii）。

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摘要

The high energetic cost of neuronal communication requires large amounts of ATP to maintain function. In mammals, oxidative phosphorylation is required to meet these energy demands and without sufficient oxygen supply neuronal hyperexcitability and excitotoxic cell death occurs. This catastrophic cascade of events does not happen in the freshwater painted turtle Chrysemys picta bellii, instead there is a coordinated downregulation of cellular ATP consuming processes to match the lower anaerobic ATP supply. To reduce the energetic burden during anoxia turtles have evolved a sophisticated network of neuroprotective mechanisms including channel arrest and spike arrest which combine to prevent membrane depolarization and activation of excessive electrical activity. The aim of my research was to identify and elucidate cellular mechanisms responsible for suppression of electrical activity in anoxic turtle dorsal cortical brain pyramidal neurons. Using electrophysiological and fluorescent imaging techniques I demonstrate for the first time that: 1) in turtle dorsal cortex a-aminobutyric acid (GABA) release increases during anoxia and enhances a unique GABAA receptor-mediated giant postsynaptic current, and shifts membrane potential to the GABA reversal potential (E GABA), reducing electrical excitability; 2) endogenous GABAergic mechanisms responsible for anoxia-tolerance also protect against a debilitating ischemic solution that mimics the cerebral fluid in the penumbral area that surrounds the infarct core; 3) in pyramidal neurons the open probability of Ca 2+-activated K+ channels decreases during anoxia and this is prevented by inhibition of protein kinase C; and 4) anoxia-mediated decreases in mitochondrial reactive oxygen species (ROS) production are sufficient to initiate a redox-sensitive inhibitory GABA signaling cascade that suppresses electrical activity. Together this research significantly contributes to our understanding of the turtle's natural anoxia-tolerant strategy in brain and highlights the integral role of channel arrest and GABAergic spike arrest in prevention of anoxic or ischemic cell damage.
机译：神经元交流的高能量成本需要大量的ATP才能维持功能。在哺乳动物中，需要氧化磷酸化来满足这些能量需求，并且在没有足够的氧气供应的情况下，神经元会过度兴奋并发生兴奋性毒性细胞死亡。这种灾难性的事件级联不会在淡水龟Chrysemys picta bellii中发生，而是细胞ATP消耗过程的协调下调，以匹配较低的无氧ATP供应。为了减少缺氧期间的能量负担，海龟进化了一种复杂的神经保护机制网络，包括通道阻滞和峰值阻滞，两者结合起来可防止膜去极化和过度电活动的激活。我的研究目的是确定和阐明负责抑制缺氧龟背皮质大脑锥体神经元电活动的细胞机制。使用电生理学和荧光成像技术，我首次证明：1）在缺氧的海龟背皮层中，α-氨基丁酸（GABA）释放增加，并增强了独特的GABAA受体介导的突触后突触大电流，并将膜电位转移至GABA反转电位（E GABA），降低电兴奋性； 2）负责耐缺氧的内源性GABA能机制还可以防止衰老的缺血性溶液，该溶液模拟梗塞核心周围半影区的脑液。 3）在锥体神经元中，缺氧时Ca 2+激活的K +通道的开放可能性降低，这可以通过抑制蛋白激酶C来防止。和4）缺氧介导的线粒体活性氧（ROS）产生的减少足以引发氧化还原敏感性抑制性GABA信号级联反应，从而抑制电活动。这些研究共同为我们理解乌龟在大脑中的天然耐缺氧策略做出了重要贡献，并强调了通道阻滞和GABA能峰值阻滞在预防缺氧或缺血性细胞损伤中的不可或缺的作用。

著录项

  • 作者

    Hogg, David William Richard.;

  • 作者单位

    University of Toronto (Canada).;

  • 授予单位 University of Toronto (Canada).;
  • 学科 Cellular biology.
  • 学位 Ph.D.
  • 年度 2015
  • 页码 172 p.
  • 总页数 172
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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