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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 ( I   K(DR) ) with a concomitant raise in current inactivation in NSC-34 neuronal cells. The dissociation constant for Flu-mediated increase of  I   K(DR)  inactivation rate was about 9.8   μ  M. Neither linopirdine (10   μ  M), NMDA (30   μ  M), nor gabazine (10   μ  M) reversed Flu-induced changes in  I   K(DR)  inactivation. Addition of Flu shifted the inactivation curve of  I   K(DR)  to a hyperpolarized potential. Cumulative inactivation for  I   K(DR)  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(DR)  amplitude and enhanced the inactivation rate of  I   K(DR) . 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(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

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