Trpv1, also known as the capsaicin receptor, is a non-selective cation channel. It is expressed by a subset of peripheral sensory neurons involved in pain sensation, and also at other neuronal and non-neuronal sites in the mammalian body. Functionally, it acts as a sensor for noxious heat (above ~42 °C), and can be activated by endogenous lipid-derived molecules, acidic solutions (pH < 6.5), pungent chemicals like capsaicin, and toxins. Structurally, its subunits have six transmembrane domains with intracellular N-and C-termini and a pore region. It plays a role in multiple processes such as pain, thermoregulation, osmoregulation, cough, and bladder function [1].

Studies with Trpv1 (-/-) mice have suggested its role in various biological processes and disease conditions. For example, in pain, thermoregulation, and osmoregulation, as well as in cough and overactive bladder [1]. In cutaneous immunity, activation of TRPV1+ neurons is sufficient to elicit a local type 17 immune response, augmenting host defense to certain pathogens [2]. In psychiatric disorders, TRPV1 blockers show anxiolytic, antipanic, and antidepressant-like effects in animal models, but their development is limited by effects on body temperature [3].

In conclusion, Trpv1 is a crucial ion channel involved in sensing noxious stimuli and regulating multiple physiological processes. Gene-knockout mouse models have been instrumental in revealing its role in pain, thermoregulation, immunity, and psychiatric disorders. Understanding Trpv1's functions provides potential therapeutic targets for treating related diseases, although challenges like hyperthermia in drug development need to be addressed [1,2,3].