Excitability of the squid giant axon revisited
Excitability of the squid giant axon revisited
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DOI：
10.1152/jn.1998.80.2.903
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发表时间：
1998-08-01
影响因子：
2.5
通讯作者：
Clay, JR
中科院分区：
文献类型：
--
作者：
Clay, JR
本文对普通鱿鱼Lolio pealei的巨型轴突的电特性进行了重新研究。这项工作的主要动机是观察到轴突的不应性明显大于神经兴奋性的标准模型的预测。具体地说，轴突只在持续的、阈值以上的刺激下发射一次。类似地，当脉冲在时间上间隔类似于10ms时，仅观察到响应于持续时间为1ms的电流脉冲序列的第一脉冲的单个动作电位。轴突对序列中的所有后续脉冲都不起作用。这些结果的潜在机制与钠和钾离子电流I-Na和I-K有关。具体地说，众所周知，钠离子通道激活与去极化电压钳制步骤中的失活是耦合的。在神经兴奋性的修正模型中，这一特征似乎是模拟脉冲序列所必需的。此外，与标准模型相比，I-K的激活曲线具有明显的电压依赖关系，特别是在其阈值附近(约-60 mV)，这有助于降低兴奋性，并且I-K的完全激活的电流-电压关系对驱动力具有非线性而不是线性的依赖关系。修正模型的另一个方面是K+在轴突和轴突周围神经胶质细胞之间的聚集/释放，即使在单个动作电位期间也是显著的，这可以解释钾平衡电位E-K与动作电位最大后超极化之间的15-20 mV差异。I-K的改变也可以解释动作电位脚部附近的电压变化的形状。
The electrical properties of the giant axon from the common squid Loligo pealei have been reexamined. The primary motivation for this work was the observation that the refractoriness of the axon was significantly greater than the predictions of the standard model of nerve excitability. In particular, the axon fired only once in response to a sustained, suprathreshold stimulus. Similarly, only a single action potential was observed in response to the first pulse of a train of 1-ms duration current pulses, when the pulses were separated in time by similar to 10 ms. The axon was refractory to all subsequent pulses in the train. The underlying mechanisms for these results concern both the sodium and potassium ion currents I-Na and I-K. Specifically, Na+ channel activation has long been known to be coupled to inactivation during a depolarizing voltage-clamp step. This feature appears to be required to simulate the pulse train results in a revised model of nerve excitability. Moreover, the activation curve for I-K has a significantly steeper voltage dependence, especially near its threshold (approximately -60 mV), than in the standard model, which contributes to reduced excitability, and the fully activated current-voltage relation for I-K has a nonlinear, rather than a linear, dependence on driving force. An additional aspect of the revised model is accumulation/depeletion of K+ in the space between the axon and the glial cells surrounding the axon, which is significant even during a single action potential and which can account for the 15-20 mV difference between the potassium equilibrium potential E-K and the maximum afterhyperpolarization of the action potential. The modifications in I-K can also account for the shape of voltage changes near the foot of the action potential.