Knockdown of the CALHM1 Gene Alleviates Allodynia in Rats With Trigeminal Neuralgia.

Abstract

OBJECTIVE: The sudden onset of trigeminal neuralgia is very similar to epilepsy. CALHM1 is associated with the development of temporal lobe epilepsy. Therefore, does CALHM1 play an important role in the pathogenesis of trigeminal neuralgia? In this study, we explored the effects of pain behaviour in rats with trigeminal neuralgia by knocking down the Calcium homeostasis modulator 1 gene. METHODS: Rats were randomly divided into the Control group, Sham group and dION-CCI group. Animal models of trigeminal neuralgia were constructed by ligating the distal infraorbital nerve of rats with a chromic gut wire; mechanical pain thresholds and spontaneous pain behaviour were measured in rats. The trigeminal spinal subnucleus caudalis was taken on day 15 postoperatively, and expression of CALHM1 was detected by qRT-PCR and western blot. The shCALHM1 group used adeno-associated viral transfection to downregulate CALHM1 expression and detected the effect of CALHM1 knockdown by immunohistochemistry. Then the dION-CCI model was established after 3 weeks. The alterations in CALHM1 expression were identified using western blot, and the modifications in pain response in rats were observed. RESULTS: The mRNA and protein expression of CALHM1 were significantly increased in the dION-CCI group. Knockdown of the CALHM1 gene attenuated the nociceptive allodynia in rats with trigeminal neuralgia. CONCLUSION: This experiment demonstrated that the occurrence of trigeminal neuralgia may be associated with increased expression of CALHM1.