| First Author | Liu Y | Year | 2022 |
| Journal | Front Mol Neurosci | Volume | 15 |
| Pages | 811441 | PubMed ID | 35359569 |
| Mgi Jnum | J:322801 | Mgi Id | MGI:7259020 |
| Doi | 10.3389/fnmol.2022.811441 | Citation | Liu Y, et al. (2022) The Slack Channel Deletion Causes Mechanical Pain Hypersensitivity in Mice. Front Mol Neurosci 15:811441 |
| abstractText | The role of the Slack (also known as Slo2.2, KNa1.1, or KCNT1) channel in pain-sensing is still in debate on which kind of pain it regulates. In the present study, we found that the Slack(-/-) mice exhibited decreased mechanical pain threshold but normal heat and cold pain sensitivity. Subsequently, X-gal staining, in situ hybridization, and immunofluorescence staining revealed high expression of the Slack channel in Isolectin B4 positive (IB4(+)) neurons in the dorsal root ganglion (DRG) and somatostatin-positive (SOM(+)) neurons in the spinal cord. Patch-clamp recordings indicated the firing frequency was increased in both small neurons in DRG and spinal SOM(+) neurons in the Slack(-/-) mice whereas no obvious slow afterhyperpolarization was observed in both WT mice and Slack(-/-) mice. Furthermore, we found Kcnt1 gene expression in spinal SOM(+) neurons in Slack(-/-) mice partially relieved the mechanical pain hypersensitivity of Slack(-/-) mice and decreased AP firing rates of the spinal SOM(+) neurons. Finally, deletion of the Slack channel in spinal SOM(+) neurons is sufficient to result in mechanical pain hypersensitivity in mice. In summary, our results suggest the important role of the Slack channel in the regulation of mechanical pain-sensing both in small neurons in DRG and SOM(+) neurons in the spinal dorsal horn. |
