Single-Channel Recording of TASK-3-like K+ Channel and Up- Regulation of TASK-3 mRNA Expression after Spinal Cord Injury in Rat Dorsal Root Ganglion Neurons.
10.4196/kjpp.2008.12.5.245
- Author:
Inseok JANG
1
;
Jun Ho LA
;
Gyu Tae KIM
;
Jeong Soon LEE
;
Eun Jin KIM
;
Eun Shin LEE
;
Su Jeong KIM
;
Jeong Min SEO
;
Sang Ho AHN
;
Jae Yong PARK
;
Seong Geun HONG
;
Dawon KANG
;
Jaehee HAN
Author Information
1. Medical Research Center for Neural Dysfunction and Department of Physiology, Jinju, Korea. dawon@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Two-pore domain K+ channel;
Dorsal root ganglion;
Spinal cord injuries;
Acidosis
- MeSH:
Acidosis;
Animals;
Brain;
Clone Cells;
Diagnosis-Related Groups;
Ganglia, Spinal;
Humans;
Hydrogen-Ion Concentration;
Kinetics;
Neurons;
Rats;
RNA, Messenger;
Spinal Cord;
Spinal Cord Injuries;
Spinal Nerve Roots;
Up-Regulation
- From:The Korean Journal of Physiology and Pharmacology
2008;12(5):245-251
- CountryRepublic of Korea
- Language:English
-
Abstract:
Single-channel recordings of TASK-1 and TASK-3, members of two-pore domain K+ channel family, have not yet been reported in dorsal root ganglion (DRG) neurons, even though their mRNA and activity in whole-cell currents have been detected in these neurons. Here, we report single-channel kinetics of the TASK-3-like K+ channel in DRG neurons and up-regulation of TASK-3 mRNA expression in tissues isolated from animals with spinal cord injury (SCI). In DRG neurons, the single-channel conductance of TASK-3-like K+ channel was 33.0+/-0.1 pS at -60 mV, and TASK-3 activity fell by 65+/-5% when the extracellular pH was changed from 7.3 to 6.3, indicating that the DRG K+ channel is similar to cloned TASK-3 channel. TASK-3 mRNA and protein levels in brain, spinal cord, and DRG were significantly higher in injured animals than in sham-operated ones. These results indicate that TASK-3 channels are expressed and functional in DRG neurons and the expression level is up-regulated following SCI, and suggest that TASK-3 channel could act as a potential background K+ channel under SCI-induced acidic condition.
