Aims: The electrical properties of Na+-activated K+ current (IK(Na)) and its contribution to spike firing has not been characterized in motor neurons. Methods: We evaluated how activation of voltage-gated K+ current (IK) at the cellular level could be coupled to Na+ influx through voltage-gated Na+ current (INa) in two motor neuron-like cells (NG108-15 and NSC-34 cells). Results: Increasing stimulation frequency altered the amplitudes of both INa and IK simultaneously. With changes in stimulation frequency, the kinetics of both INa inactivation and IK activation were well correlated at the same cell. Addition of tetrodotoxin or ranolazine reduced the amplitudes of both INa and IK simultaneously. Tefluthrin (Tef) increased the amplitudes of both INa and IK throughout the voltages ranging from -30 to + 10 mV. In cell-attached recordings, single-channel conductance from a linear current-voltage relation was 94 ± 3 pS (n = 7). Tef (10 μm) enhanced channel activity with no change in single-channel conductance. Tef increased spike firing accompanied by enhanced facilitation of spike-frequency adaptation. Riluzole (10 μm) reversed Tef-stimulated activity of KNa channels. In motor neuron-like NSC-34 cells, increasing stimulation frequency altered the kinetics of both INa and IK. Modelling studies of motor neurons were simulated to demonstrate that the magnitude of IK(Na) modulates AP firing. Conclusions: There is a direct association of Na+ and KNa channels which can provide the rapid activation of KNa channels required to regulate AP firing occurring in motor neurons.
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