The signaling role for chloride in the bidirectional communication between neurons and astrocytes.
The signaling role for chloride in the bidirectional communication between neurons and astrocytes.
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DOI:
10.1016/j.neulet.2018.01.012
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发表时间:
2019-01-10
影响因子:
2.5
通讯作者:
Mongin AA
中科院分区:
文献类型:
--
作者:
Wilson CS;Mongin AA
It is well known that the electrical signaling in neuronal networks is modulated by chloride (Cl−) fluxes via the inhibitory GABAA and glycine receptors. Here, we discuss the putative contribution of Cl− fluxes and intracellular Cl− to other forms of information transfer in the CNS, namely the bidirectional communication between neurons and astrocytes. The manuscript (i) summarizes the generic functions of Cl− in cellular physiology, (ii) recaps molecular identities and properties of Cl− transporters and channels in neurons and astrocytes, and (iii) analyzes emerging studies implicating Cl− in the modulation of neuroglial communication. The existing literature suggests that neurons can alter astrocytic Cl− levels in a number of ways; via (a) the release of neurotransmitters and activation of glial transporters that have intrinsic Cl− conductance, (b) the metabotropic receptor-driven changes in activity of the electroneutral cation-Cl− cotransporter NKCC1, and (c) transient, activity-dependent changes in glial cell volume which open the volume-regulated Cl−/anion channel VRAC. Reciprocally, astrocytes are thought to alter neuronal [Cl−]i through either (a) VRAC-mediated release of the inhibitory gliotransmitters, GABA and taurine, which open neuronal GABAA and glycine receptor/Cl− channels, or (b) the gliotransmitter-driven stimulation of NKCC1. The most important recent developments in this area are the identification of the molecular composition and functional heterogeneity of brain VRAC channels, and the discovery of a new cytosolic [Cl−] sensor – the Wnk family protein kinases. With new work in the field, our understanding of the role of Cl− in information processing within the CNS is expected to be significantly updated.
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影响因子:
6.2
作者:
Bekar, LK;Walz, W
通讯作者:
Walz, W
影响因子:
5.3
作者:
Blanz, Judith;Schweizer, Michaela;Jentsch, Thomas J.
通讯作者:
Jentsch, Thomas J.
DOI:
10.1152/physiologyonline.2000.15.6.309
发表时间:
2000-12-01
期刊:
NEWS IN PHYSIOLOGICAL SCIENCES
影响因子:
--
作者:
Delpire, E
通讯作者:
Delpire, E
影响因子:
8.3
作者:
Begum G;Yuan H;Kahle KT;Li L;Wang S;Shi Y;Shmukler BE;Yang SS;Lin SH;Alper SL;Sun D
通讯作者:
Sun D
DOI:
10.1085/jgp.81.1.53
发表时间:
1983-01
期刊:
The Journal of general physiology
影响因子:
--
作者:
Boron WF;Boulpaep EL
通讯作者:
Boulpaep EL