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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