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Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels.


ABSTRACT: 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.

SUBMITTER: Martins DF 

PROVIDER: S-EPMC10355051 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels.

Martins Daniel F DF   Sorrentino Victor V   Mazzardo-Martins Leidiane L   Reed William R WR   Santos Adair R S ARS   Gadotti Vinícius M VM   Zamponi Gerald W GW  

Molecular brain 20230718 1


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 aci  ...[more]

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