['Interaction of intravenous anaesthetic agents with voltage-dependent potassium channels significantly correlates with clinical concentrations. If potassium channels were to play an important part in anaesthesia, one might expect different effects at the molecular level of those anaesthetics that show different clinical effects. Our aim was to analyse the interaction of general anaesthetics with voltage-dependent K channels.', 'Whole cell patch-clamp experiments were analysed in detail in order to compare the effects of two clinically diverse intravenous hypnotics, ketamine and propofol, on voltage-dependent potassium channels in human neuroblastoma SH-SY5Y cells.', 'Both anaesthetics inhibited the potassium conductance in a concentration-dependent and reversible manner with IC50-values of 300 microM and 45 microM for ketamine and propofol respectively. Whereas ketamine shifted the midpoint of current activation by maximally 14 mV to more hyperpolarized potentials, propofol had the opposite effect on the activation midpoint. Current inhibition by ketamine increased with voltage but decreased with propofol at higher membrane potentials. Propofol but not ketamine induced concentration-dependent but voltage-independent decline, akin to inactivation, of the voltage-dependent potassium channels.'] Do ketamine and propofol differentially inhibit human neuronal K ( + ) channels?