%0 Journal Article
%A Breithausen, Björn
%A Kautzmann, Steffen
%A Boehlen, Anne
%A Steinhäuser, Christian
%A Henneberger, Christian
%T Limited contribution of astroglial gap junction coupling to buffering of extracellular K+ in CA1 stratum radiatum.
%J Glia
%V 68
%N 5
%@ 0894-1491
%C Bognor Regis [u.a.]
%I Wiley-Liss
%M DZNE-2020-00028
%P 918-931
%D 2019
%X Astrocytes form large networks, in which individual cells are connected via gap junctions. It is thought that this astroglial gap junction coupling contributes to the buffering of extracellular K+ increases. However, it is largely unknown how the control of extracellular K+ by astroglial gap junction coupling depends on the underlying activity patterns and on the magnitude of extracellular K+ increases. We explored this dependency in acute hippocampal slices (CA1, stratum radiatum) by direct K+ -sensitive microelectrode recordings and acute pharmacological inhibition of gap junctions. K+ transients evoked by synaptic and axonal activity were largely unaffected by acute astroglial uncoupling in slices obtained from young and adult rats. Iontophoretic K+ -application enabled us to generate K+ gradients with defined spatial properties and magnitude. By varying the K+ -iontophoresis position and protocol, we found that acute pharmacological uncoupling increases the amplitude of K+ transients once their initial amplitude exceeded  10 mM. Our experiments demonstrate that the contribution of gap junction coupling to buffering of extracellular K+ gradients is limited to large and localized K+ increases.
%K Animals
%K Astrocytes: metabolism
%K CA1 Region, Hippocampal: metabolism
%K Gap Junctions: metabolism
%K Membrane Potentials: physiology
%K Neurons: metabolism
%K Potassium: metabolism
%K Rats
%K Rats, Wistar
%K Synapses: metabolism
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:31743499
%R 10.1002/glia.23751
%U https://pub.dzne.de/record/141697