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@ARTICLE{Untiet:823823,
      author       = {Untiet, Verena and Kovermann, Peter and Gerkau, Niklas J.
                      and Gensch, Thomas and Rose, Christine R. and Fahlke,
                      Christoph},
      title        = {{G}lutamate transporter-associated anion channels adjust
                      intracellular chloride concentrations during glial
                      maturation},
      journal      = {Glia},
      volume       = {65},
      number       = {2},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {FZJ-2016-06463},
      pages        = {388–400},
      year         = {2017},
      abstract     = {Astrocytic 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.},
      cin          = {ICS-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-4-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000393669100012},
      pubmed       = {pmid:27859594},
      doi          = {10.1002/glia.23098},
      url          = {https://juser.fz-juelich.de/record/823823},
}