Abstract
In the present study we evaluated the modulation of neuronal delayed rectifier K+current (IK) by activation of ionotropic glutamate receptors. In whole-cell voltage-clamp experiments, an external application of 10-100 μM kainate suppressed the amplitude of IKfollowing an inward shift of holding current. The effect of kainate on IKwas eliminated by CN QX, an AMPA/kainate receptor antagonist, indicating that the receptor-mediated cation entry caused IKsuppression. When external Na+was completely replaced by equimolar choline+or N-methyl-D-glucamine, kainate-induced IKsuppression was abolished. Our results suggest that in cultured rat cortical neurons, AMPA/kainate receptor activation leads to an intracellular Na+increase which blocks delayed rectifier K+channels. This contributes to feed-forward excitation of neuronal cells in glutaminergic responses.
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