• Xiaoman Yuan, Siyi Han, Anne Manyande, Feng Gao, Jie Wang, Wen Zhang, and Xuebi Tian.
• Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China.
• Eur J Pain. 2023 Feb 1; 27 (2): 289302289-302.

BackgroudStudies have shown that the activation of microglia is the main mechanism of neuropathic pain. Kv1.3 channel is a novel therapeutic target for treating neuroinflammatory disorders due to its crucial role in subsets of microglial cells. As such, it may be involved in the processes of neuropathic pain, however, whether Kv1.3 plays a role in neuroinflammation following peripheral nerve injury is unclear.MethodThe spared nerve injury model (SNI) was used to establish neuropathic pain. Western blot and immunofluorescence were used to examine the effect of Kv1.3 in the SNI rats. PAP-1, a Kv1.3 specific blocker was administered to alleviate neuropathic pain in the SNI rats.ResultsNeuropathic pain and allodynia occurred after SNI, the levels of M1 (CD68, iNos) and M2 (CD206, Arg-1) phenotypes were up-regulated in the spinal cord, and the protein levels of NLRP3, caspase-1 and IL-1β were also increased. Pharmacological blocking of Kv1.3 with PAP-1 alleviated hyperpathia induced by SNI. Meanwhile, intrathecal injection of PAP-1 reduced M1 polarization and decreased NLRP3, caspase-1 and IL-1β expressions of protein levels.ConclusionOur research indicates that the Kv1.3 channel in the spinal cord contributes to neuropathic pain by promoting microglial M1 polarization and activating the NLRP3 inflammasome.© 2022 European Pain Federation - EFIC ®.

37 keywords...

hide…