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首页> 外文期刊>The European Journal of Neuroscience >Induction of pseudo-periodic oscillation in voltage-gated sodium channel properties is dependent on the duration of prolonged depolarization.
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Induction of pseudo-periodic oscillation in voltage-gated sodium channel properties is dependent on the duration of prolonged depolarization.

机译：电压门控钠通道特性中伪周期振荡的诱导取决于延长的去极化持续时间。

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Abstract The neuronal voltage-gated sodium channels play a vital role in the action potential waveform shaping and propagation. Here, we report the effects of prolonged depolarization (1-160 s) on the detailed kinetics of activation, fast inactivation and recovery from slow inactivation in the rNa(v)1.2a voltage-gated sodium channel alpha-subunit expressed in Chinese hamster ovary (CHO) cells. Wavelet analysis revealed that the duration and amplitude of a prolonged sustained depolarization altered all the steady state and kinetic parameters of the channel in a pseudo-oscillatory fashion with time-variable period and amplitude, often superimposed on a linear trend. The half steady state activation potential showed a reversible depolarizing shift of 5-10 mV with duration of prolonged depolarization, while half steady state inactivation potential showed a hyperpolarizing shift of 43-55 mV. The time periods for most of the parameters relating to activation and fast and slow inactivation, lie close to 28-30s, suggesting coupling of these kinetic processes through an oscillatory mechanism. Co-expression of the beta1-subunit affected the time periods of oscillation (close to 22 s for alpha + beta1) in steady state activation parameters. Application of a pulse protocol that mimicked paroxysmal depolarizing shift (PDS), a kind of depolarization seen in epileptic discharges, instead of a sustained depolarization, also caused oscillatory behaviour in the rNav1.2a alpha-subunit. This inherent pseudo-oscillatory mechanism may regulate excitability of the neurons, account for the epileptic discharges and subthreshold membrane potential oscillation and offer a molecular memory mechanism intrinsic to the neurons, independent of synaptic plasticity.
机译：摘要神经元电压门控钠通道在动作电位波形的形成和传播中起着至关重要的作用。在这里，我们报告延长去极化（1-160 s）对中国仓鼠卵巢中表达的rNa（v）1.2a电压门控钠通道α-亚基的活化，快速失活和从缓慢失活中恢复的详细动力学的影响（CHO）细胞。小波分析表明，长时间持续去极化的持续时间和幅度以伪振荡的方式改变了通道的所有稳态和动力学参数，其时变的幅度和时间随时间变化，通常叠加在线性趋势上。半稳态激活电位显示5-10 mV的可逆去极化位移，并具有延长的去极化持续时间，而半稳态激活电位显示43-55 mV的超极化位移。与激活以及快速和慢速失活有关的大多数参数的时间段接近28-30s，这表明这些动力学过程是通过振荡机制耦合的。在稳态激活参数中，β1亚基的共表达影响振荡的时间周期（α+β1接近22 s）。模仿阵发性去极化移位（PDS）（一种在癫痫放电中见到的去极化）而不是持续去极化的脉冲协议的应用，也引起了rNav1.2aα亚基的振荡行为。这种固有的伪振荡机制可以调节神经元的兴奋性，解决癫痫放电和阈下膜电位振荡，并提供神经元固有的分子记忆机制，而与突触可塑性无关。

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