000823823 001__ 823823
000823823 005__ 20220930130110.0
000823823 0247_ $$2doi$$a10.1002/glia.23098
000823823 0247_ $$2ISSN$$a0894-1491
000823823 0247_ $$2ISSN$$a1098-1136
000823823 0247_ $$2WOS$$aWOS:000393669100012
000823823 0247_ $$2altmetric$$aaltmetric:13791593
000823823 0247_ $$2pmid$$apmid:27859594
000823823 037__ $$aFZJ-2016-06463
000823823 082__ $$a610
000823823 1001_ $$0P:(DE-Juel1)156548$$aUntiet, Verena$$b0
000823823 245__ $$aGlutamate transporter-associated anion channels adjust intracellular chloride concentrations during glial maturation
000823823 260__ $$aBognor Regis [u.a.]$$bWiley-Liss$$c2017
000823823 3367_ $$2DRIVER$$aarticle
000823823 3367_ $$2DataCite$$aOutput Types/Journal article
000823823 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1483608047_4020
000823823 3367_ $$2BibTeX$$aARTICLE
000823823 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000823823 3367_ $$00$$2EndNote$$aJournal Article
000823823 520__ $$aAstrocytic volume regulation and neurotransmitter uptake are critically dependent on the intracellular anion concentration, but little is known about the mechanisms controlling internal anion homeostasis in these cells. Here we used fluorescence lifetime imaging microscopy (FLIM) with the chloride-sensitive dye MQAE to measure intracellular chloride concentrations in murine Bergmann glial cells in acute cerebellar slices. We found Bergmann glial [Cl−]int to be controlled by two opposing transport processes: chloride is actively accumulated by the Na+-K+-2Cl− cotransporter NKCC1, and chloride efflux through anion channels associated with excitatory amino acid transporters (EAATs) reduces [Cl−]int to values that vary upon changes in expression levels or activity of these channels. EAATs transiently form anion-selective channels during glutamate transport, and thus represent a class of ligand-gated anion channels. Age-dependent upregulation of EAATs results in a developmental chloride switch from high internal chloride concentrations (51.6 ± 2.2 mM, mean ± 95% confidence interval) during early development to adult levels (35.3 ± 0.3 mM). Simultaneous blockade of EAAT1/GLAST and EAAT2/GLT-1 increased [Cl−]int in adult glia to neonatal values. Moreover, EAAT activation by synaptic stimulations rapidly decreased [Cl−]int. Other tested chloride channels or chloride transporters do not contribute to [Cl−]int under our experimental conditions. Neither genetic removal of ClC-2 nor pharmacological block of K+-Cl− cotransporter change resting Bergmann glial [Cl−]int in acute cerebellar slices. We conclude that EAAT anion channels play an important and unexpected role in adjusting glial intracellular anion concentration during maturation and in response to cerebellar activity.
000823823 536__ $$0G:(DE-HGF)POF3-553$$a553 - Physical Basis of Diseases (POF3-553)$$cPOF3-553$$fPOF III$$x0
000823823 588__ $$aDataset connected to CrossRef
000823823 7001_ $$0P:(DE-Juel1)156374$$aKovermann, Peter$$b1
000823823 7001_ $$0P:(DE-HGF)0$$aGerkau, Niklas J.$$b2
000823823 7001_ $$0P:(DE-Juel1)131924$$aGensch, Thomas$$b3
000823823 7001_ $$0P:(DE-Juel1)IHRS-BioSoft-140013$$aRose, Christine R.$$b4
000823823 7001_ $$0P:(DE-Juel1)136837$$aFahlke, Christoph$$b5$$eCorresponding author
000823823 773__ $$0PERI:(DE-600)1474828-9$$a10.1002/glia.23098$$n2$$p388–400$$tGlia$$v65$$x0894-1491$$y2017
000823823 8767_ $$8287325$$92016-12-14$$d2017-02-17$$eColour charges$$jZahlung erfolgt$$zUSD 1650,-
000823823 909CO $$ooai:juser.fz-juelich.de:823823$$pOpenAPC$$pVDB$$popenCost
000823823 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)156548$$aForschungszentrum Jülich$$b0$$kFZJ
000823823 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)156374$$aForschungszentrum Jülich$$b1$$kFZJ
000823823 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131924$$aForschungszentrum Jülich$$b3$$kFZJ
000823823 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)IHRS-BioSoft-140013$$aForschungszentrum Jülich$$b4$$kFZJ
000823823 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)136837$$aForschungszentrum Jülich$$b5$$kFZJ
000823823 9131_ $$0G:(DE-HGF)POF3-553$$1G:(DE-HGF)POF3-550$$2G:(DE-HGF)POF3-500$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bKey Technologies$$lBioSoft – Fundamentals for future Technologies in the fields of Soft Matter and Life Sciences$$vPhysical Basis of Diseases$$x0
000823823 9141_ $$y2017
000823823 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz
000823823 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bGLIA : 2015
000823823 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000823823 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000823823 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000823823 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000823823 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000823823 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000823823 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000823823 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000823823 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000823823 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bGLIA : 2015
000823823 920__ $$lyes
000823823 9201_ $$0I:(DE-Juel1)ICS-4-20110106$$kICS-4$$lZelluläre Biophysik$$x0
000823823 980__ $$ajournal
000823823 980__ $$aVDB
000823823 980__ $$aI:(DE-Juel1)ICS-4-20110106
000823823 980__ $$aUNRESTRICTED
000823823 980__ $$aAPC
000823823 981__ $$aI:(DE-Juel1)IBI-1-20200312