Persistent sodium current and its role in epilepsy.
Persistent sodium current and its role in epilepsy.
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DOI：
10.1111/j.1535-7511.2007.00156.x
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发表时间：
2007-01-01
影响因子：
3.6
通讯作者：
Stafstrom, Carl E
中科院分区：
文献类型：
--
作者：
Stafstrom, Carl E
钠电流对于神经元放电的起始和传播是必不可少的。钠电流的改变可导致异常的神经元活动，如癫痫。瞬时电压门控钠电流介导动作电位的上升。一小部分钠电流，称为持续钠电流（I（NaP）），即使去极化时间延长，也不能显著抑制。I（NaP）在亚阈值电压范围内被激活，并且能够放大神经元对突触输入的响应并增强其重复放电能力。一个新兴的文献正在记录钠通道的突变，这是人类疾病的基础，包括癫痫。其中一些突变通过增加I（NaP）导致神经元兴奋性改变。本文综述了I（NaP）在癫痫中的病理生理作用。
Sodium currents are essential for the initiation and propagation of neuronal firing. Alterations of sodium currents can lead to abnormal neuronal activity, such as occurs in epilepsy. The transient voltage-gated sodium current mediates the upstroke of the action potential. A small fraction of sodium current, termed the persistent sodium current (I(NaP)), fails to inactivate significantly, even with prolonged depolarization. I(NaP) is activated in the subthreshold voltage range and is capable of amplifying a neuron's response to synaptic input and enhancing its repetitive firing capability. A burgeoning literature is documenting mutations in sodium channels that underlie human disease, including epilepsy. Some of these mutations lead to altered neuronal excitability by increasing I(NaP). This review focuses on the pathophysiological effects of I(NaP) in epilepsy.