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Updated: Aug 15, 2026

Controllable Ion Channel Expression through Inducible Transient Transfection
Published on: February 17, 2017
Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells
Tung-Ying Tsai1, Yu-Chuan Tsai, Sheng-Nan Wu
1Department of Anesthesiology, National Cheng Kung University Medical College, No. 1 Ta-Hsueh Road, Tainan, Tainan City 704, Taiwan, ROC.
Abstract:
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(+) (K(DR)) channels. Tramadol suppressed the amplitude of delayed rectifier K(+) current (I(K(DR))) in a concentration-dependent manner with an IC(50) values of 25 microM. Tramadol (30 microM) also shifted the steady-state inactivation of I(K(DR)) to a more negative membrane potential by approximately -15 mV. The role of the K(DR) 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 I(K(DR)) observed in this study could be partly responsible for its anti-depressant action.
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