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作 者:Yoon-Sil Yang Kyeong-Deok Kim Su-Yong Eun Sung-Cherl Jung
机构地区:[1]Department of Physiology, School of Medicine Jeju National University [2]Institute of Medical Science Jeju National University
出 处:《Neuroscience Bulletin》2014年第3期505-514,共10页神经科学通报(英文版)
基 金:supported by the 2014 Scientific Promotion Program funded by Jeju National University, Korea
摘 要:In the mammalian brain, information encoding and storage have been explained by revealing the cellular and molecular mechanisms of synaptic plasticity at various levels in the central nervous system, including the hippocampus and the cerebral cortices. The modulatory mechanisms of synaptic excitability that are correlated with neuronal tasks are fundamental factors for synaptic plasticity, and they are dependent on intracellular Ca2+-mediated signaling. In the present review, the A-type K+ (IA) channel, one of the voltage-dependent cation channels, is considered as a key player in the modulation of Ca2+ influx through synaptic NMDA receptors and their correlated signaling pathways. The cellular functions of IA channels indicate that they possibly play as integral parts of synaptic and somatic complexes, completing the initiation and stabilization of memory.In the mammalian brain, information encoding and storage have been explained by revealing the cellular and molecular mechanisms of synaptic plasticity at various levels in the central nervous system, including the hippocampus and the cerebral cortices. The modulatory mechanisms of synaptic excitability that are correlated with neuronal tasks are fundamental factors for synaptic plasticity, and they are dependent on intracellular Ca2+-mediated signaling. In the present review, the A-type K+ (IA) channel, one of the voltage-dependent cation channels, is considered as a key player in the modulation of Ca2+ influx through synaptic NMDA receptors and their correlated signaling pathways. The cellular functions of IA channels indicate that they possibly play as integral parts of synaptic and somatic complexes, completing the initiation and stabilization of memory.
关 键 词:A-type K+ channels intrinsic excitability synaptic plasticity NMDA receptors KV4.2
分 类 号:R741[医药卫生—神经病学与精神病学]
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