|Scooped by Julien Hering, PhD|
The exceptional abundance and breadth of function encountered in K+ channels has complicated efforts to untangle explicit roles in pain syndromes. Owing to advances in molecular, biochemical, electrophysiological, and genetic methods, however, we can now appreciate the involvement of specific subunits in maladaptive pain signaling after injury or inflammation. Nevertheless, there are many potential avenues of K+ involvement that have hardly been explored. It seems likely that unknown mutations in K+channel genes might contribute to inherited pain syndromes. There are many ‘silent’ K+ channel subunits for which we have little idea of whether and how they might affect pain processing. Auxiliary subunits can provide alternative substrates for pharmacological modulation; however, our understanding of these interactions in the PNS is also limited. In many chronic pain models an extensive dysregulation of several K+channels is seen, and it is unknown whether a common epigenetic control exists.