Abstract
An important characteristic of excitable cells is their ability to repolarize rapidly after a depolarizing event such as a sodium action potential. This ability is caused by several fast potassium currents such as IA and IK (ref. 1) and possibly also a fast calcium-dependent potassium current (IK(Ca))2. Suppression of only one of the potassium channels by mutation or drugs can lead to anomalous behaviour in the animal2 or to epileptic disharges3,4 in in vitro preparations. Fast potassium currents vary in their inactivation properties1, and this may be the reason why many types of potassium currents are required for the adequate functioning of neurones in various physiological conditions. Here we describe a neuronal potassium current that is activated by intracellular sodium. This current can probably be triggered by the sodium entering the neurone during a single action potential and shows little voltage inactivation. It could therefore participate in the fast repolarization process in situations where other potassium currents are partially inactivated. Because this current will be activated by any process leading to sufficient entry of sodium, it may also be triggered by sodium-mediated excitatory synaptic events. This could help to control the level of excitability in response to synaptic inputs. A sodium-dependent potassium current was recently described in heart cells5, but it was suggested that this may only become activated in pathological conditions.
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Bader, C., Bernheim, L. & Bertrand, D. Sodium-activated potassium current in cultured avian neurones. Nature 317, 540–542 (1985). https://doi.org/10.1038/317540a0
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DOI: https://doi.org/10.1038/317540a0
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