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. 2019 Feb 20;13:48. doi: 10.3389/fncel.2019.00048

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Copyright © 2019 Côme, Heubl, Schwartz, Poncer and Lévi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Homeostatic regulation of intracellular chloride via WNK1-dependent KCC2 phosphorylation. GABA_AR-dependent chloride influx inhibits WNK1 kinase activity and stabilizes KCC2 in the membrane. Increased KCC2-dependent chloride extrusion can therefore counteract efficiently chloride influx due to activation of GABAergic synapses. In conditions of decreased GABA_AR activation, a decrease in the intracellular chloride level activates WNK1. Subsequent increase in KCC2 diffusion (D) and loss of KCC2 in the membrane contribute to restore intracellular chloride concentration. From Heubl et al. (2017).