A novel acid-sensitive K+ channel in rat dorsal root ganglia neurons.

Recent studies have suggested that acid-sensitive background K+ channels such as TASK-1 and TASK-3, members of two-pore domain K+ (K2P) channel family, express and contribute to extracellular acidification-induced responses in dorsal root ganglia (DRG) neurons. However, it has remained to address whether other acid-sensitive background K+ channels are functionally expressed in DRG neurons. Here we characterized biophysical and pharmacological properties of a novel acid-sensitive background K+ channel in DRG neurons isolated from neonatal rats. We recorded an 80-pS K+ channel with a weak inward rectification current-voltage relationship in cell-attached patches in 150mM KCl bath solution. The 80-pS K+ channel was inhibited by extracellular low pH (pHo 6.3). Interestingly, the channel was similar to TASK-2 cloned from mouse and rat in biophysical and pharmacological properties. However, extracellular alkaline condition which activates TASK-2 channel, failed to activate the 80-pS K+ channel. Lidocaine and quinine more inhibited the channel activity of 80-pS K+ channel than that of TASK-2 channel. Our results suggest that the acid-sensitive 80-pS K+ channels may regulate resting membrane potential and may play a critical role in various processes such as cell metabolism, pH, and pain sensation in DRG neurons.