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Effects of analgesics and antidepressants on TREK-2 and TRESK currents

  • Park, Hyun (Department of Neurosurgery, Gyeongsang National University Hospital, College of Medicine and Institute of Health Sciences, Gyeongsang National University) ;
  • Kim, Eun-Jin (Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University) ;
  • Han, Jaehee (Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University) ;
  • Han, Jongwoo (Department of Neurosurgery, Gyeongsang National University Hospital, College of Medicine and Institute of Health Sciences, Gyeongsang National University) ;
  • Kang, Dawon (Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University)
  • 투고 : 2016.02.04
  • 심사 : 2016.05.09
  • 발행 : 2016.07.01

초록

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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