Kv2.1:: A voltage-gated K+ channel critical to dynamic control of neuronal excitability

被引：150
|
作者：
Misonou, H [1 ]
Mohapatra, DP [1 ]
Trimmer, JS [1 ]
机构：
[1] Univ Calif Davis, Sch Med, Dept Pharmacol, Davis, CA 95616 USA
来源：
NEUROTOXICOLOGY | 2005年 / 26卷 / 05期
关键词：
ion channel; phosphorylation; neuronal excitability; epilepsy; hippocampus;
D O I：
10.1016/j.neuro.2005.02.003
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Neurons use a variety of mechanisms to dynamically, control their own signaling capabilities. Regulation of voltage-dependent K+ channel localization and function has long been recognized as a major mechanism to achieve dynamic regulation of intrinsic neuronal excitability in a number of mammalian and non-mammalian neurons. Our recent evidence, together with compelling data from other laboratories, suggests that in mammalian neurons the Kv2.1 channel may play an especially prominent role in determining intrinsic neuronal excitability Kv2.1 is widely expressed in brain and composes the majority of delayed rectifier K+ current in pyramidal neurons in cortex and hippoccunpus, and is also widely expressed in interneurons. Dynamic modulation of Kv2.1 localization and junction by a mechanism involving activity-dependent Kv2.1 dephosphorylation dramatically impacts intrinsic excitability of neurons. Here we review previous studies of Kv2.1 localization and function in neurons, and summarize recent work regarding dynamic regulation of these characteristics. We also discuss possible roles of the Kv2.1 channel in neuronal and network excitability (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码：743 / 752
页数：10
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