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.
Mol Brain. 2023 Jul 18;16(1):60. doi: 10.1186/s13041-023-01049-3.
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.
本研究旨在探讨 Cav3.2 T 型通道在介导关节松动术（JM）治疗的抗痛觉过敏活性中的相对贡献。我们使用慢性缩窄性损伤模型（CCI）诱导雄性小鼠周围神经病变和慢性疼痛，然后进行 JM。我们证明 JM 产生持久的机械性抗痛觉过敏，而在 Cav3.2 缺失小鼠中则被消除。此外，我们发现 JM 表现出与脂肪酸酰胺水解酶抑制剂 URB597 相似的镇痛谱，这表明可能涉及内源性大麻素的作用机制趋同。总的来说，我们的研究结果加深了我们对 JM 产生镇痛作用的机制的理解。
