TY - JOUR
T1 - A novel acid-sensitive K+ channel in rat dorsal root ganglia neurons
AU - La, Jun Ho
AU - Kang, Dawon
AU - Park, Jae Yong
AU - Hong, Seong Geun
AU - Han, Jaehee
N1 - Funding Information:
This work was supported by the Korea Research Foundation Grant (KRF-2004-005-E00008) and partially supported by grants No. R01-2004-000-10443-0 and R13-2005-012-01002-0 from the Basic Research Program of the Korea Science & Engineering Foundation.
PY - 2006/10/9
Y1 - 2006/10/9
N2 - 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 150 mM 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.
AB - 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 150 mM 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.
KW - Acid-sensitive channel
KW - Background K channels
KW - Dorsal root ganglion neurons
KW - TASK-2
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U2 - 10.1016/j.neulet.2006.07.039
DO - 10.1016/j.neulet.2006.07.039
M3 - Article
C2 - 16904821
AN - SCOPUS:33748328115
SN - 0304-3940
VL - 406
SP - 244
EP - 249
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -