Preliminary study of calcium homeostasis modulator 1 involved in trigeminal neuralgia

Background: The aim of this study was to observe the changes in the expression of calcium homeostasis modulator 1 (CALHM1) in the trigeminal nucleus of the trigeminal neuralgia (TN) rats with the infraorbital nerve-chronic constrictive nerve injury (ION-CCI) and to explore the role of CALHM1 in TN.Methods: Thirty SD rats were randomly assigned to 5 groups, namely normal control group (Control group), sham operation group (Sham group), TN model group (ION-CCI group), ruthenium red treatment group (RuR group) and control group of ruthenium red (NS group), with 6 rats in each group. An animal model was established by loosely ligating the rat's infraorbital nerve with a chrome gut in the ION-CCI group, while mice in the sham group were only exposed to the nerve and did not receive ligature. The rats in the RuR group were intraperitoneally injected with 0.5 mg/kg of CALHM1 inhibitor ruthenium red on the 9th day after the infraorbital nerve ligation, while the rats in NS group were intraperitoneally injected with an equal volume of normal saline on the 9th day after surgery. All experimental rats were tested for pain behavior 1 day before surgery, 1, 3, 5, 7, 9, 11 and 14 days after surgery, including the mechanical pain threshold of VonFrey filament in the trigeminal innervated skin area and number of faces captured in video recording. The expression of CALHM1 in the trigeminal spinal nucleus was detected on the 15th day after operation in all experimental groups.Results: The expression of CALHM1 in the trigeminal spinal nucleus of the ION-CCI group was significantly higher than that of control group and sham group on the 3rd and 15th day after modeling. The intraperitoneal injection of CALHM1 inhibitor ruthenium red increased the mechanical pain threshold of ION-CCI rats and significantly reduced the number of scratches, but did not change the expression of CALHM1 in the trigeminal spinal nucleus.Conclusion: The expression of CALHM1 protein in the trigeminal spinal nucleus is involved in the central sensitization of TN pain, which can be induced by elevated expression. Moreover, the hyperalgesia can be improved by using CALHM1 inhibitor.