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Limited contribution of astroglial gap junction coupling to buffering of extracellular K + in CA1 stratum radiatum
Author(s) -
Breithausen Björn,
Kautzmann Steffen,
Boehlen Anne,
Steinhäuser Christian,
Henneberger Christian
Publication year - 2020
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23751
Subject(s) - gap junction , extracellular , coupling (piping) , biophysics , iontophoresis , biology , neuroscience , heptanol , hippocampal formation , microelectrode , materials science , intracellular , physics , microbiology and biotechnology , electrode , metallurgy , quantum mechanics
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.