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Sodium-Activated Potassium Channels Are Functionally Coupled to Persistent Sodium Currents

We report a novel coupled system of sodium-activated potassium currents (IKNa) and persistent sodium currents (INaP), the components of which are widely distributed throughout the brain. Its existence and importance has not been previously recognized. Although IKNa was known to exist in many cell types, the source of Na+ which activates IKNa remained a mystery. We now show in single membrane patches generated from the somas of rat neurons that sodium influx through INaP is sufficient for activation of KNa channels, without substantial contribution from the transient sodium current or bulk [Na+]i. INaP was found to be active at cell membrane resting potentials, a finding that may explain why IKNa can be evoked from negative holding potentials. These results show an unanticipated role for INaP in activating a negative feedback system countering the excitable effects INaP; the interrelatedness of INaP and IKNa suggests new ways neurons can tune their excitability.