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海马CA1锥体神经元树突中组成型激活的G蛋白门控内向整流钾通道。

Constitutively active G-protein-gated inwardly rectifying K+ channels in dendrites of hippocampal CA1 pyramidal neurons.

作者信息

Chen Xixi, Johnston Daniel

机构信息

Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

J Neurosci. 2005 Apr 13;25(15):3787-92. doi: 10.1523/JNEUROSCI.5312-04.2005.

Abstract

A diversity of ion channels contributes to the active properties of neuronal dendrites. From the apical dendrites of hippocampal CA1 pyramidal neurons, we recorded inwardly rectifying K+ channels with a single-channel conductance of 33 pS. The inwardly rectifying K+ channels were constitutively active at the resting membrane potential. The amount of constitutive channel activity was significantly larger in the apical dendrites than in the soma. Activities of these inwardly rectifying K+ channels were inhibited by Ba2+ (200 microM) and tertiapin (10 nM), both of which are believed to block G-protein-coupled inwardly rectifying K+ (GIRK) channels. Intracellularly applied GTPgammaS (20 microM) during dual dendritic recordings significantly increased constitutive channel activity. Baclofen (20 microM), an agonist for the G-protein-coupled GABA(B) receptor, also significantly increased the level of channel activity. Therefore, these channels are GIRK channels, which are constitutively active at rest in the apical dendrites of CA1 pyramidal neurons and can be further activated via G-protein-coupled neurotransmitter receptors.

摘要

多种离子通道促成了神经元树突的主动特性。我们从海马体CA1锥体神经元的顶端树突记录到单通道电导为33 pS的内向整流钾通道。内向整流钾通道在静息膜电位时即呈组成性激活状态。顶端树突中组成性通道活性的量显著大于胞体中的量。这些内向整流钾通道的活性受到Ba2+(200 microM)和特律平(10 nM)的抑制,这两种物质都被认为可阻断G蛋白偶联内向整流钾(GIRK)通道。在双树突记录期间细胞内施加GTPγS(20 microM)可显著增加组成性通道活性。巴氯芬(20 microM),一种G蛋白偶联GABA(B)受体的激动剂,也显著提高了通道活性水平。因此,这些通道是GIRK通道,它们在CA1锥体神经元顶端树突中静息时即呈组成性激活状态,并可通过G蛋白偶联神经递质受体进一步激活。

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