ABSTRACT
Sodium channel Nav1. 7 is one of the subtypes of voltage-gated sodium channel. Most of it is expressed on the nociceptors of small C fibers in dorsal root ganglion (DRG). It has the characteristics of slow opening and slow closing of inactivation. It can produce a large amount of ramp current, reduce the threshold of action potential in sensory neurons, and amplify the external small and slow depolarization ramp current. Thus, it can increase the excitability of neurons and play a key role in the generation, transmission and regulation of pain. With the deepening of genetic research, Nav1. 7 channel has become a particularly attractive drug target in new analgesic therapy due to its function acquired mutation and function deletion mutation. However, the study found that Nav1. 7 channel improves neuronal excitability and participates in neuropathic pain through different ways in neuropathic pain caused by different factors, which has brought great obstacles to the research and development of Nav1. 7 selective inhibitors. Although the existing Nav1. 7 selective inhibitors have effective analgesic effects without obvious side effects or addiction problems, it is extremely difficult to find Nav1. 7 selective ligands. In addition, the existing Nav1. 7 selective inhibitors also differ in inhibitory efficacy, targeting, safety and feasibility due to different types of neuropathic pain. It is suggested that finding the general mechanism of Nav1. 7 channel acting on different neuropathic pain or the specific receptor binding site of Nav1. 7 channel may be the main direction of the research and development of Nav1. 7 selective inhibitors in the future. This paper briefly reviews the main role of Nav1. 7 channel in neuropathic pain caused by different factors.