Abstract:Sodium channel Nav1.3, a voltage-gated sodium channel subtype, is encoded by SCN3A gene and is sensitive to tetrodotoxin(TTX). Nav1.3 channel current is characterized by rapid activation, rapid deactivation and rapid recovery from the deactivation state to maintain high-frequency discharge. It can be activated during slow ramp depolarization and generate sustained sodium current, which amplifies neuronal excitability and plays an important role in the generation and conduction of neural electrical signals. Studies have found that the missense mutation of Nav1.3 is common to the current changes caused by some nerve injuries, leading to abnormal neuronal firing in various ways, and participating in and regulating the occurrence of hyperalgesia. This article reviews the related mechanisms of Nav1.3 involved in pathological pain (inflammatory pain, neuropathic pain, etc.), discusses the relationship between the expression changes of Nav1.3 in nerve sites and the pain-sensitive phenotype, the upstream and downstream signals of Nav1.3 regulated by various cytokines and their receptors, and the differences in the changes of different pathological pain, etc. To analyze the role and mechanism of Nav1.3 in pathologic pain, and to explore the possibility of Nav1.3 as an analgesic target.
