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10.1038/s41467-017-01749-0 http://scihub22266oqcxt.onion/10.1038/s41467-017-01749-0 C5701213!5701213 !29176664     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29176664 &cmd=llinks): Failed to open stream: HTTP request failed! 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GABA(A) receptor dependent synaptic inhibition rapidly tunes KCC2 activity via the Cl(-)-sensitive WNK1 kinase |pdf=|usr=}}{{29176664 }} gab.com Text GABA(A) receptor dependent synaptic inhibition rapidly tunes KCC2 activity via the Cl(-)-sensitive WNK1 kinase JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29176664 #FOAvip The K(+)-Cl(-) co-transporter KCC2 (SLC12A5) tunes the efficacy of GABA(A) receptor-mediated transmission by regulating the intraneuronal chloride concentration [Cl(-)](i). KCC2 undergoes activity-dependent regulation in both physiological and pathological conditions. The regulation of KCC2 by synaptic excitation is well documented; however, whether the transporter is regulated by synaptic inhibition is unknown. Here we report a mechanism of KCC2 regulation by GABA(A) receptor (GABA(A)R)-mediated transmission in mature hippocampal neurons. Enhancing GABA(A)R-mediated inhibition confines KCC2 to the plasma membrane, while antagonizing inhibition reduces KCC2 surface expression by increasing the lateral diffusion and endocytosis of the transporter. This mechanism utilizes Cl(-) as an intracellular secondary messenger and is dependent on phosphorylation of KCC2 at threonines 906 and 1007 by the Cl(-)-sensing kinase WNK1. We propose this mechanism contributes to the homeostasis of synaptic inhibition by rapidly adjusting neuronal [Cl(-)](i) to GABA(A)R activity. Twit Text FOAVip GABA(A) receptor dependent synaptic inhibition rapidly tunes KCC2 activity via the Cl(-)-sensitive WNK1 kinase ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29176664 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29176664 #FOAvip English Wikipedia <ref>{{Cite pmid|29176664 }}</ref> GABA(A) receptor dependent synaptic inhibition rapidly tunes KCC2 activity via the Cl(-)-sensitive WNK1 kinase #MMPMID29176664 Heubl M ; Zhang J ; Pressey JC ; Al Awabdh S ; Renner M ; Gomez-Castro F ; Moutkine I ; Eugène E ; Russeau M ; Kahle KT ; Poncer JC ; Lévi S Nat Commun 2017[Nov]; 8 (1 ): 1776 PMID29176664 show ga The K(+)-Cl(-) co-transporter KCC2 (SLC12A5) tunes the efficacy of GABA(A) receptor-mediated transmission by regulating the intraneuronal chloride concentration [Cl(-)](i). KCC2 undergoes activity-dependent regulation in both physiological and pathological conditions. The regulation of KCC2 by synaptic excitation is well documented; however, whether the transporter is regulated by synaptic inhibition is unknown. Here we report a mechanism of KCC2 regulation by GABA(A) receptor (GABA(A)R)-mediated transmission in mature hippocampal neurons. Enhancing GABA(A)R-mediated inhibition confines KCC2 to the plasma membrane, while antagonizing inhibition reduces KCC2 surface expression by increasing the lateral diffusion and endocytosis of the transporter. This mechanism utilizes Cl(-) as an intracellular secondary messenger and is dependent on phosphorylation of KCC2 at threonines 906 and 1007 by the Cl(-)-sensing kinase WNK1. We propose this mechanism contributes to the homeostasis of synaptic inhibition by rapidly adjusting neuronal [Cl(-)](i) to GABA(A)R activity. |Animals [MESH] |Cell Membrane/genetics/metabolism [MESH] |Cells, Cultured [MESH] |Chlorides/*metabolism [MESH] |Endocytosis [MESH] |Hippocampus/cytology/enzymology/metabolism [MESH] |K Cl- Cotransporters [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neurons/enzymology/metabolism [MESH] |Phosphorylation [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptors, GABA-A/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Symporters/genetics/*metabolism [MESH] |Synaptic Transmission [MESH]GABA(A) receptor dependent synaptic inhibition rapidly tunes KCC2 acti(epmc).pdf DeepDyve Pubget Overpricing