Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels

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dc.contributor.authorMartins, Daniel F.
dc.contributor.authorSorrentino, Victor
dc.contributor.authorMazzardo-Martins, Leidiane
dc.contributor.authorReed, William R.
dc.contributor.authorSantos, Adair R. S.
dc.contributor.authorGadotti, Vinícius M.
dc.contributor.authorZamponi, Gerald W.
dc.date.accessioned2023-07-23T00:03:11Z
dc.date.available2023-07-23T00:03:11Z
dc.date.issued2023-07-18
dc.date.updated2023-07-23T00:03:11Z
dc.description.abstractAbstract 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.
dc.identifier.citationMolecular Brain. 2023 Jul 18;16(1):60
dc.identifier.urihttps://doi.org/10.1186/s13041-023-01049-3
dc.identifier.urihttps://hdl.handle.net/1880/116784
dc.identifier.urihttps://dx.doi.org/10.11575/PRISM/41626
dc.language.rfc3066en
dc.rights.holderThe Author(s)
dc.titleAntihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels
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