A considerable number of individuals are diagnosed with idiopathic trigeminal neuralgia. In order to achieve a more complete understanding of the pathophysiology, it is essential to adopt a range of novel approaches and utilize new animal models. This study investigated changes in the messenger RNA (mRNA) expression of ion-channels in a newly developed animal model of trigeminal neuropathic pain induced by cervical spinal dorsal horn compression. Eighteen rabbits were randomly assigned into three groups (spinal cord compression, sham, and control groups), and a previously developed animal model was applied. Quantitative polymerase chain reaction was applied to examine the genetic expression of Na, K, and Ca channels in the cervical dorsal horn, trigeminal ganglion, and infraorbital nerve. The mRNA expression levels of SCN8A and SCN9A exhibited a marked increase in the infraorbital nerve of the spinal cord compression group when compared to the sham group. Furthermore, the mRNA expression levels of CACNA1C, KCNK1, and SCN9A demonstrated a significant increase in all investigated regions when compared to the control group. The present findings indicate the potential critical involvement of Nav1.6 and Nav1.7 in the pathogenesis of trigeminal neuropathic pain. However, the potential involvement of the CaV2.1, CaV1.2, and K2P1.1 channels cannot be ruled out at this juncture.