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

Research output: Contribution to journalArticle

23 Citations (Scopus)

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+ (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.

Original languageEnglish
Pages (from-to)597-601
Number of pages5
JournalEuropean Journal of Pain
Volume10
Issue number7
DOIs
Publication statusPublished - 2006 Oct 1

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Tramadol
Potassium
Membrane Potentials
Action Potentials
Inhibitory Concentration 50
Analgesics
Ions
Neurons
Pain
Cell Line
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

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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+ (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.",
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Tramadol-induced blockade of delayed rectifier potassium current in NG108-15 neuronal cells. / Tsai, Tung Ying; Tsai, Yu-Chuan; Wu, Sheng-Nan; Liu, Yen-Chin.

In: European Journal of Pain, Vol. 10, No. 7, 01.10.2006, p. 597-601.

Research output: Contribution to journalArticle

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AB - 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.

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