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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 (IK(DR)) with a concomitant raise in current inactivation in NSC-34 neuronal cells. The dissociation constant for Flu-mediated increase of IK(DR) inactivation rate was about 9.8 μM. Neither linopirdine (10 μM), NMDA (30 μM), nor gabazine (10 μM) reversed Flu-induced changes in IK(DR) inactivation. Addition of Flu shifted the inactivation curve of IK(DR) to a hyperpolarized potential. Cumulative inactivation for IK(DR) was elevated in the presence of this compound. Flu increased the amplitude of M-type K+ current (IK(M)) and produced a leftward shift in the activation curve of IK(M). In another neuronal cells (NG108-15), Flu reduced IK(DR) amplitude and enhanced the inactivation rate of IK(DR). The results suggest that Flu acts as an open-channel blocker of delayed-rectifier K+ channels in motor neurons. Flu-induced block of IK(DR) 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.

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