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急性窒息时猫脊髓运动神经元的细胞内记录。

Intracellular recording from cat spinal motoneurones during acute asphyxia.

作者信息

Collewijn H, Van Harreveld A

出版信息

J Physiol. 1966 Jul;185(1):1-14. doi: 10.1113/jphysiol.1966.sp007968.

Abstract
  1. Changes in membrane and action potentials of cat spinal motoneurones during acute asphyxiation and re-oxygenation were recorded with an intracellular technique.2. The asphyxial potential of the grey matter, which develops in the first 2-2.5 min of asphyxiation, can be expected to interfere with the membrane potential record. After correcting for this effect a gradual depolarization of the soma at a rate of 3-4 mV/min was found, commencing within a fraction of a minute after the start of asphyxiation.3. The orthodromic responses of the motoneurones were the most vulnerable to O(2) lack. They failed earlier than the responses to antidromic and to direct excitation of the cell through the micro-electrode. After failure of the orthodromic spike an excitatory post-synaptic potential remained for a short time. Failure of antidromic excitation began by the dropping out of the some dendritic potential, followed by the arrest of the initial segment response.4. It was concluded that the early arrest of orthodromic excitation is caused by presynaptic failure.5. All changes in membrane and action potentials were completely reversible by re-oxygenation after periods of asphyxia lasting from 4 to 6 min. The orthodromic response recovered markedly slower than the antidromic and direct ones.
摘要
  1. 采用细胞内记录技术,记录了猫脊髓运动神经元在急性窒息和复氧过程中膜电位和动作电位的变化。

  2. 灰质的窒息电位在窒息开始后的2 - 2.5分钟内出现,预计会干扰膜电位记录。校正此效应后,发现胞体在窒息开始后不到一分钟内开始以3 - 4 mV/分钟的速率逐渐去极化。

  3. 运动神经元的顺向反应对缺氧最为敏感。它们比逆向反应以及通过微电极对细胞进行直接刺激的反应更早消失。顺向峰电位消失后,兴奋性突触后电位仍会短暂存在。逆向兴奋的消失始于一些树突电位的消失,随后是始段反应的停止。

  4. 得出的结论是,顺向兴奋的早期停止是由突触前功能障碍引起的。

  5. 在持续4至6分钟的窒息期后,通过复氧,膜电位和动作电位的所有变化都是完全可逆的。顺向反应的恢复明显慢于逆向反应和直接刺激反应。

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Influence of asphyxia on membrane potential level and action potentials of spinal motoand interneurons.
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