Premium
Tramadol‐induced blockade of delayed rectifier potassium current in NG108‐15 neuronal cells
Author(s) -
Tsai TungYing,
Tsai YuChuan,
Wu ShengNan,
Liu YenChin
Publication year - 2006
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2005.09.001
Subject(s) - tramadol , potassium channel , analgesic , chemistry , blockade , inward rectifier potassium ion channel , ion channel , pharmacology , potassium channel blocker , membrane potential , patch clamp , electrophysiology , biophysics , anesthesia , medicine , receptor , biochemistry , biology
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 μM. Tramadol (30 μM) 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.