Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels

The present study was undertaken to explore the relative contributions of Cav3.2 T-type channels to mediating the antihyperalgesic activity of joint manipulation (JM) therapy. We used the chronic constriction injury model (CCI) to induce peripheral neuropathy and chronic pain in male mice, followed by JM. We demonstrate that JM produces long-lasting mechanical anti-hyperalgesia that is abolished in Cav3.2 null mice. Moreover, we found that JM displays a similar analgesic profile as the fatty acid amide hydrolase inhibitor URB597, suggesting a possible converging mechanism of action involving endocannabinoids. Overall, our findings advance our understanding of the mechanisms through which JM produces analgesia.

Automated summary

The present study aimed to investigate the role of Cav3.2 T-type channels in mediating the antihyperalgesic effects of joint manipulation (JM) therapy. Using a chronic constriction injury model in mice, we demonstrated that JM produced long-lasting mechanical antihyperalgesia, which was abolished in Cav3.2 null mice. Additionally, we found that JM displayed a similar analgesic profile to the fatty acid amide hydrolase inhibitor URB597, suggesting a possible shared mechanism of action involving endocannabinoids. Overall, our findings contribute to the understanding of the analgesic mechanisms of JM.