2. Academic Validation
  3. Structure and Function of Sodium Channel Nav1.3 in Neurological Disorders

Structure and Function of Sodium Channel Nav1.3 in Neurological Disorders

  • Cell Mol Neurobiol. 2023 Mar;43(2):575-584. doi: 10.1007/s10571-022-01211-w.
Sheng Liao # 1 2 3,  Tao Liu # 1 2 3,  Ruozhu Yang 1 2 3,  Weitong Tan 1 2 3,  Jiaqi Gu 1 2 3,  Meichun Deng 4 5 6
Affiliations

Affiliations

  • 1 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.
  • 2 Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
  • 3 Hunan Key Laboratory of Animal Models for Human Diseases, Hunan Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, 410013, Hunan, China.
  • 4 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. [email protected].
  • 5 Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China. [email protected].
  • 6 Hunan Key Laboratory of Animal Models for Human Diseases, Hunan Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, 410013, Hunan, China. [email protected].
  • # Contributed equally.
PMID: 35332400 DOI: 10.1007/s10571-022-01211-w
Abstract

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.

Keywords

Epilepsy; Nav1.3; Neuropathic pain; SCN3A; Voltage-gated sodium channel.

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