Scaling in neuronal intrinsic excitability cooperates with synaptic transmission to control the information storage.This regulation of neuronal plasticity can be affected by alterations in neuronal inputs and accomplished by modulation of voltage-dependent ion channels.Here,we report that enhanced excitatory input negatively regulated neuronal excitability.Enhanced excitatory input by glutamate,electric field stimulation or high K+ increased transient outward K+ current,whereas did not affect the delayed rectifier K+ current in rat cortical neurons.The increase in the K+ current density was ascribed to the cytoplasmic membrane translocation of voltage-dependent K+ channel 4.2,which was mediated by N-methyl-D-aspartate type of glutamate receptor.Furthermore,enhanced excitatory input inhibited neuronal excitability.Taken together,our results suggest that excitatory neurotransmission affects neuronal excitability via regulation of the K+ channel membrane translocation.