Effects of analgesics and antidepressants on TREK-2 and TRESK currentsopen access
- Authors
- Park, Hyun; Kim, Eun-Jin; Han, Jaehee; Han, Jongwoo; Kang, Dawon
- Issue Date
- Jul-2016
- Publisher
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Keywords
- Analgesics; Background potassium channels; Pain
- Citation
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.20, no.4, pp.379 - 385
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Volume
- 20
- Number
- 4
- Start Page
- 379
- End Page
- 385
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/15407
- DOI
- 10.4196/kjpp.2016.20.4.379
- ISSN
- 1226-4512
- 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 specific activators of TREK-2 and TRESK may be beneficial 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.
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