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Objective Trigeminal neuralgia is the most common maxillofacial pain syndrome, and its etiology has not been fully understood. In this paper, we focus on the role and expression of G protein-gated inwardly rectifying potassium channel (GIRK) protein in trigeminal neuralgia to provide a new direction for the treatment of trigeminal neuralgia. Methods An animal model of trigeminal neuralgia in mice was established by infraorbital nerve transection surgery, and its mechanical abnormal pain was measured by using Von Frey; the number of facial scratches was recorded to measure its spontaneous pain; the expression of GIRK protein in trigeminal ganglion was detected by Western Blot. Results Our research discovered that after trigeminal nerve injury in mice, both mechanical abnormal pain and spontaneous pain were significantly enhanced at 3-21 days postoperatively compared to controls, while both GIRK1-3 protein levels were downregulated in the trigeminal ganglion. Conclusion Trigeminal neuralgia model in mice was successfully established， and suggesting that GIRK may play a significant role in trigeminal neuralgia after nerve injury.