Liao Sheng, Liu Tao, Yang Ruozhu, Tan Weitong, Gu Jiaqi, Deng Meichun
Department of Biochemistry and Molecular Biology & Hunan Province Key Laboratory of Basic and Applied Hematology, School of Life Sciences, Central South University, Changsha, 410013, Hunan, China.
Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Cell Mol Neurobiol. 2023 Mar;43(2):575-584. doi: 10.1007/s10571-022-01211-w. Epub 2022 Mar 24.
Nav1.3, encoded by the SCN3A gene, is a voltage-gated sodium channel on the cell membrane. It is expressed abundantly in the fetal brain but little in the normal adult brain. It is involved in the generation and conduction of action potentials in excitable cells. Nav1.3 plays an important role in many neurological diseases. The aim of this review is to summarize new findings about Nav1.3 in the field of neurology. Many mutations of SCN3A can lead to neuronal hyperexcitability and then cause epilepsy. The rapid recovery from inactivation and slow closed-state inactivation kinetics of Nav1.3 leads to a reduced activation threshold of the channel and a high frequency of firing of neurons. Hyperactivity of Nav1.3 also induces increased excitability of sensory neurons, a lower nociceptive threshold, and neuropathic pain. This review summarizes the structure and the function of Nav1.3 and focuses on its relationship with epilepsy and neuropathic pain.
由SCN3A基因编码的Nav1.3是一种细胞膜上的电压门控钠通道。它在胎儿大脑中大量表达,但在正常成人大脑中表达较少。它参与可兴奋细胞动作电位的产生和传导。Nav1.3在许多神经系统疾病中起重要作用。本综述的目的是总结神经学领域中关于Nav1.3的新发现。SCN3A的许多突变可导致神经元过度兴奋,进而引起癫痫。Nav1.3从失活状态的快速恢复以及缓慢的关闭状态失活动力学导致通道的激活阈值降低和神经元高频放电。Nav1.3的过度活跃还会诱导感觉神经元兴奋性增加、痛觉阈值降低和神经性疼痛。本综述总结了Nav1.3的结构和功能,并重点关注其与癫痫和神经性疼痛的关系。