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The Kv4.2 mediates excitatory activity‐dependent regulation of neuronal excitability in rat cortical neurons
Author(s) -
Shen Bin,
Zhou Kechun,
Yang Shenglian,
Xu Tianle,
Wang Yizheng
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.05179.x
Subject(s) - neuroscience , excitatory postsynaptic potential , cortical neurons , premovement neuronal activity , biology , chemistry , inhibitory postsynaptic potential
Neuronal excitability can cooperate 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. In this study, 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 cultured cortical neurons. Both the voltage‐dependent K + channel 4.2 and 4.3 subunits contributed to the increase. The increase in the K + current density by Kv4.2 was ascribed to its cytoplasmic membrane translocation, which was mediated by NMDA type of glutamate receptor. Furthermore, enhanced excitatory input inhibited neuronal excitability. Taken together, our results suggest that excitatory neurotransmission affects neuronal excitability via the regulation of the K + channel membrane translocation.