Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells

Tung Ying Tsai, Yu Chuan Tsai, Sheng Nan Wu, Yen Chin Liu

研究成果: Article同行評審

25 引文 斯高帕斯(Scopus)

摘要

Tramadol is a centrally acting analgesic drug used mainly in the moderate to severe pain control. In this study, the effects of this agent on ion currents of NG108-15 neuronal cells were investigated. This cell line expresses Kv3.1a mRNAs and exhibits the activity of delayed rectifier K+ (KDR) channels. Tramadol suppressed the amplitude of delayed rectifier K+ current (IK(DR)) in a concentration-dependent manner with an IC50 values of 25 μM. Tramadol (30 μM) also shifted the steady-state inactivation of IK(DR) to a more negative membrane potential by approximately -15 mV. The role of the KDR channel, particularly as a member of the Kv3 superfamily, is to stabilize the resting potential and to reduce the width of action potentials in the time-coding neurons. Tramadol-induced block of IK(DR) observed in this study could be partly responsible for its anti-depressant action.

原文English
頁(從 - 到)597
頁數1
期刊European Journal of Pain
10
發行號7
DOIs
出版狀態Published - 2006 十月

All Science Journal Classification (ASJC) codes

  • 麻醉與疼痛醫學

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