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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 148403, 10 pages
Research Article

Evidence for Inhibitory Effects of Flupirtine, a Centrally Acting Analgesic, on Delayed Rectifier K+ Currents in Motor Neuron-Like Cells

1Department of Physiology, National Cheng Kung University Medical College, Tainan City 70101, Taiwan
2Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan City 70101, Taiwan
3Department of Psychology, National Cheng Kung University, Tainan City 70101, Taiwan
4Department of Pediatrics, Kaohsiung Medical University Chung-Ho Memorial Hospital, Kaohsiung City, Taiwan
5Department of Pharmacology, Kaohsiung Medical University, Kaohsiung City 80708, Taiwan

Received 10 May 2012; Accepted 18 June 2012

Academic Editor: Adair Roberto Soares Santos

Copyright © 2012 Sheng-Nan Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Flupirtine (Flu), a triaminopyridine derivative, is a centrally acting, non-opiate analgesic agent. In this study, effects of Flu on K + currents were explored in two types of motor neuron-like cells. Cell exposure to Flu decreased the amplitude of delayed rectifier K + current ( 𝐼 K ( D R ) ) with a concomitant raise in current inactivation in NSC-34 neuronal cells. The dissociation constant for Flu-mediated increase of 𝐼 K ( D R ) inactivation rate was about 9.8 μM. Neither linopirdine (10 μM), NMDA (30 μM), nor gabazine (10 μM) reversed Flu-induced changes in 𝐼 K ( D R ) inactivation. Addition of Flu shifted the inactivation curve of 𝐼 K ( D R ) to a hyperpolarized potential. Cumulative inactivation for 𝐼 K ( D R ) was elevated in the presence of this compound. Flu increased the amplitude of M-type K + current ( 𝐼 K ( M ) ) and produced a leftward shift in the activation curve of 𝐼 K ( M ) . In another neuronal cells (NG108-15), Flu reduced 𝐼 K ( D R ) amplitude and enhanced the inactivation rate of 𝐼 K ( D R ) . The results suggest that Flu acts as an open-channel blocker of delayed-rectifier K + channels in motor neurons. Flu-induced block of 𝐼 K ( D R ) is unlinked to binding to NMDA or GABA receptors and the effects of this agent on K + channels are not limited to its action on M-type K + channels.