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) the 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.
The signaling role for chloride in the bidirectional communication between neurons and astrocytes.
Published 2018 in Neuroscience Letters
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- Publication year
2018
- Venue
Neuroscience Letters
- Publication date
2018-01-09
- Fields of study
Biology, Medicine, Chemistry
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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