Effects of analgesics and antidepressants on TREK-2 and TRESK currents.
10.4196/kjpp.2016.20.4.379
- Author:
Hyun PARK
1
;
Eun Jin KIM
;
Jaehee HAN
;
Jongwoo HAN
;
Dawon KANG
Author Information
1. Department of Neurosurgery, Gyeongsang National University Hospital, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea.
- Publication Type:Original Article
- Keywords:
Analgesics;
Background potassium channels;
Pain
- MeSH:
Acetaminophen;
Amitriptyline;
Analgesics*;
Antidepressive Agents*;
Bupropion;
Citalopram;
Fluoxetine;
Humans;
Ibuprofen;
Membrane Potentials;
Potassium Channels, Tandem Pore Domain;
Sensory Receptor Cells;
Spinal Cord
- From:The Korean Journal of Physiology and Pharmacology
2016;20(4):379-385
- CountryRepublic of Korea
- Language:English
-
Abstract:
TWIK-related K+ channel-2 (TREK-2) and TWIK-related spinal cord K+ (TRESK) channel are members of two-pore domain K+ channel family. They are well expressed and help to set the resting membrane potential in sensory neurons. Modulation of TREK-2 and TRESK channels are involved in the pathogenesis of pain, and specifi c activators of TREK-2 and TRESK may be benefi cial for the treatment of pain symptoms. However, the effect of commonly used analgesics on TREK-2 and TRESK channels are not known. Here, we investigated the effect of analgesics on TREK-2 and TRESK channels. The effects of analgesics were examined in HEK cells transfected with TREK-2 or TRESK. Amitriptyline, citalopram, escitalopram, and fluoxetine significantly inhibited TREK-2 and TRESK currents in HEK cells (p<0.05, n=10). Acetaminophen, ibuprofen, nabumetone, and bupropion inhibited TRESK, but had no effect on TREK-2. These results show that all analgesics tested in this study inhibit TRESK activity. Further study is needed to identify the mechanisms by which the analgesics modulate TREK-2 and TRESK differently.
