K v 2.1 and silent K v subunits underlie the delayed rectifier K + current in cultured small mouse DRG neurons

• Published in: American Journal of Physiology: Cell Physiology 2009-06, Vol.296 (6), p.C1271-C1278
• Main Authors: Bocksteins, Elke, Raes, Adam L., Van de Vijver, Gerda, Bruyns, Tine, Van Bogaert, Pierre-Paul, Snyders, Dirk J.
• Format: Article
• Language: English
• ISSN: 0363-6143; 1522-1563
• DOI: 10.1152/ajpcell.00088.2009

Silent voltage-gated K + (K v ) subunits interact with K v 2 subunits and primarily modulate the voltage dependence of inactivation of these heterotetrameric channels. Both K v 2 and silent K v subunits are expressed in the mammalian nervous system, but little is known about their expression and function in sensory neurons. This study reports the presence of K v 2.1, K v 2.2, and silent subunit K v 6.1, K v 8.1, K v 9.1, K v 9.2, and K v 9.3 mRNA in mouse dorsal root ganglia (DRG). Immunocytochemistry confirmed the protein expression of K v 2.x and K v 9.x subunits in cultured small DRG neurons. To investigate if K v 2 and silent K v subunits are underlying the delayed rectifier K + current ( I K ) in these neurons, K v 2-mediated currents were isolated by the extracellular application of rStromatoxin-1 (ScTx) or by the intracellular application of K v 2 antibodies. Both ScTx- and anti-K v 2.1-sensitive currents displayed two components in their voltage dependence of inactivation. Together, both components accounted for approximately two-thirds of I K . A comparison with results obtained in heterologous expression systems suggests that one component reflects homotetrameric K v 2.1 channels, whereas the other component represents heterotetrameric K v 2.1/silent K v channels. These observations support a physiological role for silent K v subunits in small DRG neurons.