Pharmakologisches Institut für Naturwissenschaftler, Goethe-Universität, Fachbereich Biochemie, Chemie und Pharmazie, 60438 Frankfurt am Main, Germany; Institut für Pharmakologie und Toxikologie, Universität Witten/Herdecke, ZBAF, 58453 Witten, Germany.
Pharmakologisches Institut für Naturwissenschaftler, Goethe-Universität, Fachbereich Biochemie, Chemie und Pharmazie, 60438 Frankfurt am Main, Germany.
Neuropharmacology. 2017 Oct;125:386-395. doi: 10.1016/j.neuropharm.2017.08.021. Epub 2017 Aug 18.
Intermediate conductance calcium-activated potassium channels (K3.1) have been recently implicated in pain processing. However, the functional role and localization of K3.1 in the nociceptive system are largely unknown. We here characterized the behavior of mice lacking K3.1 (K3.1) in various pain models and analyzed the expression pattern of K3.1 in dorsal root ganglia (DRG) and the spinal cord. K3.1 mice demonstrated normal behavioral responses in models of acute nociceptive, persistent inflammatory, and persistent neuropathic pain. However, their behavioral responses to noxious chemical stimuli such as formalin and capsaicin were increased. Accordingly, formalin-induced nociceptive behavior was increased in wild-type mice after administration of the K3.1 inhibitor TRAM-34. In situ hybridization experiments detected K3.1 in most DRG satellite glial cells, in a minority of DRG neurons, and in ependymal cells lining the central canal of the spinal cord. Together, our data point to a specific inhibitory role of K3.1 for the processing of noxious chemical stimuli.
中介电导钙激活钾通道（K3.1）最近被牵涉到疼痛处理中。然而，K3.1 在伤害感受系统中的功能作用和定位在很大程度上仍是未知的。我们在此描述了缺失 K3.1（K3.1）的小鼠在各种疼痛模型中的行为，并分析了 K3.1 在背根神经节（DRG）和脊髓中的表达模式。K3.1 小鼠在急性伤害感受、持续性炎症和持续性神经病理性疼痛模型中表现出正常的行为反应。然而，它们对甲醛和辣椒素等有害化学刺激的行为反应增加了。相应地，在给予 K3.1 抑制剂 TRAM-34 后，野生型小鼠的甲醛诱导的疼痛行为增加了。原位杂交实验检测到 K3.1 在大多数 DRG 卫星胶质细胞、少数 DRG 神经元和脊髓中央管的室管膜细胞中表达。总的来说，我们的数据表明 K3.1 对有害化学刺激的处理具有特定的抑制作用。
