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Calcium current inactivation in identified neurones of Helix aspersa.庭院蜗牛特定神经元中的钙电流失活
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Calcium-mediated control of Ca and K currents.钙介导的钙电流和钾电流调控
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Properties of a Ca2+ activated K+ conductance in Helix neurones investigated by intracellular Ca2+ ionophoresis.通过细胞内钙离子载体法研究的海兔神经元中钙离子激活钾离子电导的特性。
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Electrophysiology of mammalian inferior olivary neurones in vitro. Different types of voltage-dependent ionic conductances.体外培养的哺乳动物下橄榄核神经元的电生理学。不同类型的电压依赖性离子电导。
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The axon reaction: a review of the principal features of perikaryal responses to axon injury.轴突反应:对轴突损伤后胞体反应主要特征的综述
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豚鼠迷走神经运动核轴突切断后变性神经元的电生理学

Electrophysiology of degenerating neurones in the vagal motor nucleus of the guinea-pig following axotomy.

作者信息

Laiwand R, Werman R, Yarom Y

机构信息

Department of Neurobiology, Hebrew University, Jerusalem, Israel.

出版信息

J Physiol. 1988 Oct;404:749-66. doi: 10.1113/jphysiol.1988.sp017317.

DOI:10.1113/jphysiol.1988.sp017317
PMID:2855353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190853/
Abstract
  1. The electrophysiological properties of motoneurones in the dorsal motor nucleus of the vagus in the guinea-pig were studied at different times following cervical vagotomy. The results were compared both to normal neurones and to results obtained at the same time from intact neurones located in the contralateral nucleus. 2. The input resistances of axotomized neurones are significantly higher than those of normal neurones (66 +/- 29 compared to 45 +/- 17 M omega). This difference was seen during the first month following axotomy without any sign of a time-dependent process. On the other hand, no change in resting potential was observed. 3. Significant reduction in action potential amplitude was observed 1 month after axotomy (from 97.8 +/- 8 to 87 +/- 7 mV) and was followed by slow recovery lasting more than 1 year. Neither the Na+ conductance nor the voltage-dependent K+ conductance responsible for the fast rise and fall of the action potential, respectively, were affected by axotomy. 4. One month after axotomy the action potential duration in axotomized neurones was found to be shorter than that of normal neurones (0.9 +/- 0.1 ms compared to 1.1 +/- 0.04 ms). We show that this decrease in duration reflects a reduction in the depolarizing hump on the falling phase of the action potential, which is known to express the Ca2+ conductance activated during the action potential. A slow recovery of the spike duration was observed, although an age-dependent reduction in duration was also observed in neurones in the contralateral nucleus. 5. Two K+ conductances, the Ca2+-dependent and the A type, decrease 1 month after axotomy and follow a similar time course of recovery to that of the reduction in action potential duration and amplitude. 6. The firing pattern of axotomized neurones undergoes profound alteration, manifested as an increase in firing duration as a response to a rectangular current pulse. Examination of these alterations reveals that the reduction in both K+ conductances is responsible for the observed changes. 7. The results are discussed within the framework of the degenerative response known to take place in the nucleus following axotomy. We hypothesize that the observed phenomena reflect an increase in intracellular Ca2+ concentration which, in turn, inactivates the Ca2+ and K+ conductances. Furthermore this rise in intracellular Ca2+ may eventually be responsible for cell death.
摘要
  1. 在豚鼠颈迷走神经切断后的不同时间,研究了迷走神经背核运动神经元的电生理特性。将结果与正常神经元以及同时从对侧核中完整神经元获得的结果进行比较。2. 轴突切断的神经元的输入电阻显著高于正常神经元(分别为66±29与45±17 MΩ)。这种差异在轴突切断后的第一个月就出现了,没有任何时间依赖性过程的迹象。另一方面,静息电位没有观察到变化。3. 轴突切断后1个月观察到动作电位幅度显著降低(从97.8±8降至87±7 mV),随后是持续超过1年的缓慢恢复。分别负责动作电位快速上升和下降的Na⁺电导和电压依赖性K⁺电导均不受轴突切断的影响。4. 轴突切断后1个月,发现轴突切断的神经元的动作电位持续时间比正常神经元短(分别为0.9±0.1 ms与1.1±0.04 ms)。我们表明,这种持续时间的减少反映了动作电位下降相去极化峰的减少,已知该去极化峰表达动作电位期间激活的Ca²⁺电导。观察到动作电位持续时间的缓慢恢复,尽管对侧核中的神经元也观察到了与年龄相关的持续时间减少。5. 两种K⁺电导,即Ca²⁺依赖性和A 型,在轴突切断后1个月降低,并遵循与动作电位持续时间和幅度减少相似的恢复时间进程。6. 轴突切断的神经元的放电模式发生了深刻改变,表现为对矩形电流脉冲的反应中放电持续时间增加。对这些改变的检查表明,两种K⁺电导的降低是观察到的变化的原因。7. 在已知轴突切断后核中发生的退行性反应的框架内讨论了这些结果。我们假设观察到的现象反映了细胞内Ca²⁺浓度的增加,这反过来又使Ca²⁺和K⁺电导失活。此外,细胞内Ca²⁺的这种升高最终可能导致细胞死亡。