K⁺ channels are transmembrane proteins expressed in many excitable and non-excitable cells. Functional entities are formed by the tetrameric assembly of α subunits which could be done in a homomeric or heteromeric fashion. In addition, the association of β subunits is also required for the proper function of K⁺channels. Various splice variants are also expressed, thereby complicating the picture^1,2.

K⁺ channels belonging to the K_V9 subfamily resemble the delayed-rectifier class of K⁺ channel a subunits. These channels include six transmembrane domains, an ion selective pore, a leucine zipper and positively charged amino acids in S4 the voltage sensor domain. Interestingly, both K_V9.1 and K_V9.3 channels are electrically silent delayed rectifying K⁺ channels. However, they are responsible for modifying the activity of other K⁺ channels such as that of K_V2.1, yielding currents different from those of K_V2.1 on its own¹.

K_V9.1 is mainly expressed in the brain, human lens epithelial cells, kidney, prostate and testis. That of K_V9.3 is more generalized and ubiquitous¹.

Interestingly, a polymorphism in the gene encoding for K_V9.1 was identified and associated with high risks of suffering from neuropathic pain³. Evidently, additional work needs to be done to evaluate and decipher the role of K_V9.1 (if at all) in chronic pain states.