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@ARTICLE{Engels:897220,
      author       = {Engels, Miriam and Kalia, Manu and Rahmati, Sarah and
                      Petersilie, Laura and Kovermann, Peter and van Putten,
                      Michel J. A. M. and Rose, Christine R. and Meijer, Hil G. E.
                      and Gensch, Thomas and Fahlke, Christoph},
      title        = {{G}lial {C}hloride {H}omeostasis {U}nder {T}ransient
                      {I}schemic {S}tress},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {15},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2021-03682},
      pages        = {735300},
      year         = {2021},
      abstract     = {High water permeabilities permit rapid adjustments of glial
                      volume upon changes in external and internal osmolarity, and
                      pathologically altered intracellular chloride concentrations
                      ([Cl–]int) and glial cell swelling are often assumed to
                      represent early events in ischemia, infections, or traumatic
                      brain injury. Experimental data for glial [Cl–]int are
                      lacking for most brain regions, under normal as well as
                      under pathological conditions. We measured [Cl–]int in
                      hippocampal and neocortical astrocytes and in hippocampal
                      radial glia-like (RGL) cells in acute murine brain slices
                      using fluorescence lifetime imaging microscopy with the
                      chloride-sensitive dye MQAE at room temperature. We observed
                      substantial heterogeneity in baseline [Cl–]int, ranging
                      from 14.0 ± 2.0 mM in neocortical astrocytes to 28.4 ± 3.0
                      mM in dentate gyrus astrocytes. Chloride accumulation by the
                      Na+-K+-2Cl– cotransporter (NKCC1) and chloride outward
                      transport (efflux) through K+-Cl– cotransporters (KCC1 and
                      KCC3) or excitatory amino acid transporter (EAAT) anion
                      channels control [Cl–]int to variable extent in distinct
                      brain regions. In hippocampal astrocytes, blocking NKCC1
                      decreased [Cl–]int, whereas KCC or EAAT anion channel
                      inhibition had little effect. In contrast, neocortical
                      astrocytic or RGL [Cl–]int was very sensitive to block of
                      chloride outward transport, but not to NKCC1 inhibition.
                      Mathematical modeling demonstrated that higher numbers of
                      NKCC1 and KCC transporters can account for lower [Cl–]int
                      in neocortical than in hippocampal astrocytes. Energy
                      depletion mimicking ischemia for up to 10 min did not result
                      in pronounced changes in [Cl–]int in any of the tested
                      glial cell types. However, [Cl–]int changes occurred under
                      ischemic conditions after blocking selected anion
                      transporters. We conclude that stimulated chloride
                      accumulation and chloride efflux compensate for each other
                      and prevent glial swelling under transient energy
                      deprivation.},
      cin          = {IBI-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-1-20200312},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34602981},
      UT           = {WOS:000702038800001},
      doi          = {10.3389/fncel.2021.735300},
      url          = {https://juser.fz-juelich.de/record/897220},
}