Trpm3, a member of the TRP family, encodes proteins forming cation-permeable ion channels on the plasma membrane. It has multiple unique features, such as a large number of isoforms generated mainly by alternative splicing. An intronic microRNA (miR-204) is co-transcribed with Trpm3, increasing the functional complexity of the Trpm3 locus. TRPM3 channels are involved in pathways like sensing noxious heat, modulating insulin release, and secreting inflammatory cytokines [1].

In acute oxaliplatin-induced peripheral neuropathic pain studies, TRPM3-deficient mice did not develop cold and mechano hypersensitivity as control mice did. The levels of protein ERK, a neuronal activity marker, were significantly reduced in dorsal root ganglion neurons from TRPM3-deficient mice after oxaliplatin administration. Also, the injection of a TRPM3 antagonist effectively reduced pain behavior in mice with acute oxaliplatin-induced peripheral neuropathy, indicating 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 release. The study of Trpm3-deficient mouse models has revealed its role in acute oxaliplatin-induced peripheral neuropathic pain, suggesting it could be a valuable therapeutic target in this disease area.