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The activation of P2×4R activates microglia, opens the ion channels on the cell membrane (mainly calcium influx), activates intracellular related signal pathways in microglia (such as AKT, JNK), releases various injurious factors (such as TNF-a, IL-18, IL-10), induces and promotes nerve cell damage (such as neurons, astrocytes), and causes pain. While the application of P2 × 4 receptor-related antagonists (such as 5-BDBD and NP-1815-PX) can inhibit the activity of P2 × 4R, reduce its over-expression, decrease the release of injury factors, and relieve pain. Neuropathic pain (NPP) is a common symptom of most diseases in clinic, which seriously affects the mental health of patients and brings certain pain to patients. Due to its pathological mechanism is very complicated, and thus, its treatment has been one of the challenges in the field of medicine. Therefore, exploring the pathogenesis and treatment approach of NPP has aroused the interest of many researchers. ATP is an important energy information substance, which participates in the signal transmission in the body. The P2 × 4 receptor (P2 × 4R) is dependent on ATP ligand-gated cationic channel receptor, which can be activated by ATP and plays an important role in the transmission of information in the nervous system and the formation of pain. In this paper, we provide a comprehensive review of the structure and function of the P2 × 4R gene. We also discuss the pathogenesis of NPP and the intrinsic relationship between P2 × 4R and NPP. Moreover, we explore the pharmacological properties of P2 × 4R antagonists or inhibitors used as targeted therapies for NPP. [ABSTRACT FROM AUTHOR]