Potassium channels: Newly found players in synaptic plasticity

Potassium channels: Newly found players in synaptic plasticity
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DOI:
10.1177/1073858408315041
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发表时间:
2008-06-01
期刊:
影响因子:
5.6
通讯作者:
Hoffman, Dax A.
Hoffman, Dax A.
中科院分区:
医学2区
文献类型:
--
作者:
Kim, Jinhyun;Hoffman, Dax A.

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现代神经科学研究的主要问题之一是大脑获取、存储和回忆记忆的分子和细胞机制。几十年来,个体突触输入强度的调节(突触可塑性)一直是细胞信息存储的前沿候选机制,最近获得了一些直接的支持证据。到目前为止,对负责改变突触强度的分子机制的研究主要集中在神经递质受体本身(AMPAR和NMDAR)的运输和特性上。然而,最近的证据表明,受体激活后,突触输入受到突触定位的K+通道的调节。因此,了解这些通道的生物物理特性和亚细胞定位(密度和分布)以及它们的特性是如何调节的是至关重要的。在这里,我们将回顾最近的研究结果表明,两种不同类型的K+通道(A型和小电导,钙激活的K+通道),超出了他们的传统作用,在调节动作电位放电,有助于调节突触强度在海马。此外,我们还讨论了这些通道的性质和表达的调节如何有助于突触可塑性。
One of the major issues for modern neuroscience research concerns the molecular and cellular mechanisms that underlie the acquisition, storage, and recollection of memories by the brain. Regulation of the strength of individual synaptic inputs (synaptic plasticity) has, for decades, been the front-running candidate mechanism for cellular information storage, with some direct supporting evidence recently obtained. Research into the molecular mechanisms responsible for changing synaptic strength has, to date, primarily focused on trafficking and properties of the neurotransmitter receptors themselves (AMPARs and NMDARs). However, recent evidence indicates that, subsequent to receptor activation, synaptic inputs are subject to regulation by synaptically located K+ channels. It is therefore critical to understand the biophysical properties and subcellular localization (density and distribution) of these channels and how their properties are modulated. Here we will review recent findings showing that two different classes of K+ channels (A-type and small conductance, Ca2+-activated K+ channels), beyond their traditional role in regulating action potential firing, contribute to the regulation of synaptic strength in the hippocampus. In addition, we discuss how modulation of these channels' properties and expression might contribute to synaptic plasticity.