% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@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},
}