Trpm3, a member of the TRP family, encodes proteins forming cation-permeable ion channels on the plasma membrane [1]. It has unique features like generating numerous isoforms mainly through alternative splicing. An intronic microRNA (miR-204) co-transcribed with Trpm3 increases its functional complexity. TRPM3 channels are involved in pathways such as sensing noxious heat, modulating insulin release, and cytokine secretion, and are expressed in various tissues like nociceptive neurons, pancreatic beta cells, and vascular smooth muscle cells [1]. Adequate pharmacological and genetic tools make it possible to study Trpm3 further.

In in vivo behavioral studies using an acute oxaliplatin model for chemotherapy-induced peripheral neuropathic pain (CIPNP), control mice developed cold and mechano-hypersensitivity, while TRPM3 -deficient mice did not. Also, the level of protein ERK, a neuronal activity marker, was significantly reduced in dorsal root ganglion neurons from TRPM3 -deficient mice after oxaliplatin administration. Intraperitoneal injection of a TRPM3 antagonist effectively reduced oxaliplatin-induced pain behavior, suggesting TRPM3 as a potential target for treating neuropathic pain in chemotherapy patients [2].

In conclusion, Trpm3 is crucial for functions like thermosensation, pain transduction, and regulation of insulin and cytokine secretion. The study of TRPM3 -deficient mouse models has revealed its potential role in chemotherapy-induced peripheral neuropathic pain, offering new insights into the treatment of this condition.