Kv2 channels form delayed-rectifier potassium channels in situ

A non inactivating potassium current known as the delayed rectifier plays a major role in membrane repolarization during an action potential. Whereas several candidate genes exist that code for potassium current, the identiti es of the molecular isotypes that are responsible in situ for membrane repo larization remain unidentified. We report that Kv2 channels play a major ro le in action potential repolarization. Kv2 channel elimination resulted in a reduction of the density of noninactivating potassium current and a prolo nged impulse duration. In contrast, suppression of noninactivating current carried by Kv1 channels was much less effective in increasing action potent ial durations. Thus, whereas different potassium channels encode sustained potassium current, their contributions to action potential repolarization v ary and require direct examination in situ. Our results indicate that Kv2 s ubunits function as classic delayed-rectifier channels in vertebrate neuron s.