Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels

Molecular Brain

Micro Report

William R. Reed¹  Gerald W. Zamponi²  Vinícius M. Gadotti²  Victor Sorrentino³  Leidiane Mazzardo-Martins⁴  Daniel F. Martins⁴  Adair R. S. Santos⁵ 

[1] Department of Physical Therapy, Rehabilitation Science Program, University of Alabama at Birmingham, Birmingham, AL, USA;Departments of Clinical Neurosciences, and Physiology & Pharmacology, Hotchkiss Brain Institute, Alberta Children’s Hospital Research Institute, University of Calgary, T2N 4N1, Calgary, AB, Canada;Experimental Neuroscience Laboratory (LaNEx), Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Palhoça, SC, Brazil;Experimental Neuroscience Laboratory (LaNEx), Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Palhoça, SC, Brazil;Programa de Pós-Graduação em Neurociências, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário-Trindade, Florianópolis, SC, Brazil;Programa de Pós-Graduação em Neurociências, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário-Trindade, Florianópolis, SC, Brazil;

关键词: Joint mobilization therapy;    Cav3.2 channel;    Mechanical hyperalgesia;    Analgesia;   

DOI  :  10.1186/s13041-023-01049-3

 received in 2023-06-11, accepted in 2023-07-12,  发布年份 2023

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY   
© The Author(s) 2023

【 图 表 】

Fig. 1