Migraine is a neurological disease that is very common in society and is characterized by symptoms such as severe headaches, nausea, and sensitivity to light and sound. Absence from work, decreased productivity and healthcare costs due to migraine impose a high economic burden on patients and countries. For this reason, research on preventing or treating this disease continues intensively towards understanding migraine pathophysiology and drug discovery. In studies investigating migraine pathophysiology, new specific targets have emerged in drug development, such as the Calcitonin Gene and Peptide (CGRP) pathway. Current studies show that imbalance in neuronal calcium (Ca²⁺) homeostasis is effective in the pathogenesis of neurodegenerative disorders. Transient receptor potential (TRP) cation channels are non-selective cation channels and integral proteins that are widely expressed in the membranes of cells and organelles, especially in mammalian cells, and are involved in various cellular functions. It is known that transient receptor potential (TRP) channels cause neuronal apoptosis in cases of oxidative stress and Ca²⁺ homeostasis in neurological diseases. Therefore, TRP channels in migraine may be useful in preventing cellular damage due to oxidative stress in neurological disorders. TRPV1 (Transient receptor potential family, transient receptor potential vanilloid receptor1) is a non-selective ion channel protein first expressed in the dorsal root, trigeminal and nodos ganglia. Therefore, it is clear that TRPV1 channels have an important role in migraine treatment. Additionally, it has been shown that by using TRPV1 channel antagonists, Ca²⁺ influx into the intracellular environment can be prevented and thus cell homeostasis can be preserved. In this review, we examined the role of the TRPV1 channel in migraine based on recent studies.