TRPM1 is a constitutively open nonselective cation channel that mediates influx of divalent cations including Ca²⁺, Mg²⁺, Mn²⁺, Ba²⁺, and Ni²⁺, while remaining impermeable to zinc ions 1. The channel can form heteromultimeric complexes with TRPM3 that conduct both calcium and zinc 1. TRPM1 plays an essential role in retinal phototransduction, specifically in ON-bipolar cell depolarization 23. The channel operates within the mGluR6 signaling cascade: in darkness, glutamate release activates GRM6, leading to G-protein-mediated TRPM1 channel inactivation; light-induced glutamate decrease deactivates GRM6, allowing channel opening and membrane depolarization 4. Ultrastructurally, TRPM1 localizes to ON-bipolar cell dendrite tips invaginating photoreceptor terminals, and is expressed in select rod photoreceptors 5. Clinically, TRPM1 mutations cause congenital stationary night blindness (CSNB), characterized by early-onset night blindness due to rod dysfunction 4. Additionally, TRPM1 serves as a retinal autoantigen in paraneoplastic retinopathy and is implicated in melanoma pathogenesis and metastasis suppression 46. Recent genome-wide association studies identify TRPM1 as a putative causal gene for age-related macular degeneration 7.