Upregulation of TACAN in the trigeminal ganglion affects pain transduction in acute pulpitis.

OBJECTIVE: Acute pulpitis is one of the common causes of tooth pain. TACAN (Tmem120a) is a newly identified ion channel that senses mechanical pain. In this experiment, we studied the expression of the TACAN ion channel in the trigeminal ganglia in a rat model of pulpitis to explore the correlation between the expression of this ion channel and inflammatory pain. DESIGN: Lipopolysaccharide was used to induce acute pulpitis in rats, and pulpitis was assessed histologically. The facial pain threshold of the rats was measured by the von Frey test. TACAN mRNA expression in rat dental pulp and the trigeminal nerve was measured by qPCR, and TACAN protein expression in the trigeminal ganglia was evaluated by western blot analysis and immunofluorescence. Antisense oligonucleotides were used to reduce TACAN protein expression in the trigeminal ganglia, and the change in the pain threshold in the rats with acute pulpitis was determined. RESULTS: The results showed that the TACAN transcript level in rat pulp tissue increased under inflammatory conditions, and we proved that pulpitis increased TACAN protein expression in the rat ipsilateral trigeminal ganglia. The facial pain threshold was decreased in rats with pulpitis. A short-term decrease in TACAN protein expression could improve the pain threshold. CONCLUSIONS: With the development of pulpitis after bacterial infection, the upregulation of TACAN expression in the trigeminal ganglia promoted pain sensitivity. A short-term reduction in TACAN expression relieved pain. Therefore, this study indicated that TACAN is a potential target channel for new analgesics.