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本文引用的文献

1
Plasticity of astroglial networks in olfactory glomeruli.嗅小球中天冬氨酸能神经元网络的可塑性。
Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18442-6. doi: 10.1073/pnas.1107386108. Epub 2011 Oct 13.
2
NBCe1 mediates the acute stimulation of astrocytic glycolysis by extracellular K+.NBCe1 介导细胞外 K+对星形胶质细胞糖酵解的急性刺激。
J Neurosci. 2011 Oct 5;31(40):14264-71. doi: 10.1523/JNEUROSCI.2310-11.2011.
3
Targeting pannexin1 improves seizure outcome.靶向连接蛋白 1 可改善癫痫发作结局。
PLoS One. 2011;6(9):e25178. doi: 10.1371/journal.pone.0025178. Epub 2011 Sep 16.
4
Pannexin channels are not gap junction hemichannels.缝隙连接通道不是连接子通道。
Channels (Austin). 2011 May-Jun;5(3):193-7. doi: 10.4161/chan.5.3.15765. Epub 2011 May 1.
5
Implication of Kir4.1 channel in excess potassium clearance: an in vivo study on anesthetized glial-conditional Kir4.1 knock-out mice.Kir4.1 通道在钾离子清除过多中的作用:麻醉条件性 Kir4.1 敲除小鼠的体内研究。
J Neurosci. 2010 Nov 24;30(47):15769-77. doi: 10.1523/JNEUROSCI.2078-10.2010.
6
Electrical coupling of astrocytes in rat hippocampal slices under physiological and simulated ischemic conditions.在生理和模拟缺血条件下大鼠海马切片中海马星形细胞的电偶联。
Glia. 2010 Mar;58(4):481-93. doi: 10.1002/glia.20939.
7
The pannexin 1 channel activates the inflammasome in neurons and astrocytes.泛连接蛋白1通道可激活神经元和星形胶质细胞中的炎性小体。
J Biol Chem. 2009 Jul 3;284(27):18143-51. doi: 10.1074/jbc.M109.004804. Epub 2009 May 5.
8
The neuronal connexin36 interacts with and is phosphorylated by CaMKII in a way similar to CaMKII interaction with glutamate receptors.神经元连接蛋白36与钙/钙调蛋白依赖性蛋白激酶II(CaMKII)相互作用并被其磷酸化,其方式类似于CaMKII与谷氨酸受体的相互作用。
Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20964-9. doi: 10.1073/pnas.0805408105. Epub 2008 Dec 18.
9
Connexins, pannexins, innexins: novel roles of "hemi-channels".连接蛋白、泛连接蛋白、间隙连接蛋白:“半通道”的新作用。
Pflugers Arch. 2009 Apr;457(6):1207-26. doi: 10.1007/s00424-008-0591-5. Epub 2008 Oct 14.
10
Connexin and pannexin mediated cell-cell communication.连接蛋白和泛连接蛋白介导细胞间通讯。
Neuron Glia Biol. 2007 Aug;3(3):199-208. doi: 10.1017/S1740925X08000069.

细胞外钾离子和星形胶质细胞通过缝隙连接蛋白和连接蛋白通道的信号转导。

Extracellular K⁺ and astrocyte signaling via connexin and pannexin channels.

机构信息

Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

Neurochem Res. 2012 Nov;37(11):2310-6. doi: 10.1007/s11064-012-0759-4. Epub 2012 Apr 6.

DOI:10.1007/s11064-012-0759-4
PMID:22481627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3489984/
Abstract

Astrocytes utilize two major pathways to achieve long distance intercellular communication. One pathway involves direct gap junction mediated signal transmission and the other consists of release of ATP through pannexin channels and excitation of purinergic receptors on nearby cells. Elevated extracellular potassium to levels occurring around hyperactive neurons affects both gap junction and pannexin1 channels. The action on Cx43 gap junctions is to increase intercellular coupling for a period that long outlasts the stimulus. This long term increase in coupling, termed "LINC", is mediated through calcium and calmodulin dependent activation of calmodulin dependent kinase (CaMK). Pannexin1 can be activated by elevations in extracellular potassium through a mechanism that is quite different. In this case, potassium shifts activation potentials to more physiological range, thereby allowing channel opening at resting or slightly depolarized potentials. Enhanced activity of both these channel types by elevations in extracellular potassium of the magnitude occurring during periods of high neuronal activity likely has profound effects on intercellular signaling among astrocytes in the nervous system.

摘要

星形胶质细胞利用两种主要途径实现长距离细胞间通讯。一种途径涉及直接缝隙连接介导的信号传递,另一种途径则包括通过连接蛋白通道释放 ATP 以及兴奋附近细胞上的嘌呤能受体。升高至过度活跃神经元周围发生的水平的细胞外钾影响缝隙连接和连接蛋白 1 通道。对 Cx43 缝隙连接的作用是在很长一段时间内增加细胞间偶联,远远超过刺激时间。这种称为“LINC”的长期耦合增加是通过钙和钙调蛋白依赖性钙调蛋白依赖性激酶(CaMK)的激活介导的。通过一种完全不同的机制,细胞外钾的升高可以激活连接蛋白 1。在这种情况下,钾会将激活电位转移到更接近生理范围,从而使通道在静息或轻微去极化电位下打开。在神经元活动高的时期,细胞外钾升高增强这两种通道类型的活性,这可能对神经系统中星形胶质细胞之间的细胞间信号传递产生深远影响。