首页> 美国卫生研究院文献>The Journal of Physiology >Electrophysiology of degenerating neurones in the vagal motor nucleus of the guinea-pig following axotomy.
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Electrophysiology of degenerating neurones in the vagal motor nucleus of the guinea-pig following axotomy.

机译:轴切术后豚鼠迷走神经核中退化神经元的电生理。

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摘要

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.
机译:1.研究了在豚鼠宫颈迷走神经切断术后不同时间,迷走神经背运动核中运动神经元的电生理特性。将结果与正常神经元以及从对侧核中完整神经元同时获得的结果进行比较。 2.轴突化神经元的输入电阻显着高于正常神经元(66 +/- 29相比45 +/- 17 MΩ)。在轴切术后的第一个月内观察到这种差异,没有任何时间依赖性过程的迹象。另一方面,未观察到静息电位的变化。 3.切开术后1个月观察到动作电位幅度显着降低(从97.8 +/- 8降至87 +/- 7 mV),随后缓慢恢复,持续了1年以上。轴切术既不影响动作电位快速上升和下降的Na +电导,也不依赖电压依赖性K +电导。 4.切开切断后一个月,发现切开后的神经元的动作电位持续时间短于正常神经元(0.9 +/- 0.1毫秒,而1.1 +/- 0.04毫秒)。我们表明,持续时间的减少反映了动作电位下降阶段的去极化峰的减少,已知这表示在动作电位期间激活的Ca2 +电导。观察到刺突持续时间的缓慢恢复,尽管在对侧核神经元中也观察到了持续时间的年龄依赖性降低。 5.轴切术后1个月,两种K +电导(依赖于Ca2 +)和A型电导率降低,并遵循与动作电位持续时间和幅度降低相似的恢复时间。 6.轴突化神经元的放电模式发生了深刻的变化,表现为随着对矩形电流脉冲的响应,放电持续时间的增加。对这些变化的检查表明,两个K +电导的降低是观察到的变化的原因。 7.结果在已知的轴切术后发生在核内的变性反应的框架内讨论。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 +的升高可能最终导致细胞死亡。

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