TY  - JOUR
AU  - Breithausen, Björn
AU  - Kautzmann, Steffen
AU  - Boehlen, Anne
AU  - Steinhäuser, Christian
AU  - Henneberger, Christian
TI  - Limited contribution of astroglial gap junction coupling to buffering of extracellular K+ in CA1 stratum radiatum.
JO  - Glia
VL  - 68
IS  - 5
SN  - 0894-1491
CY  - Bognor Regis [u.a.]
PB  - Wiley-Liss
M1  - DZNE-2020-00028
SP  - 918-931
PY  - 2019
AB  - 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.
KW  - Animals
KW  - Astrocytes: metabolism
KW  - CA1 Region, Hippocampal: metabolism
KW  - Gap Junctions: metabolism
KW  - Membrane Potentials: physiology
KW  - Neurons: metabolism
KW  - Potassium: metabolism
KW  - Rats
KW  - Rats, Wistar
KW  - Synapses: metabolism
LB  - PUB:(DE-HGF)16
C6  - pmid:31743499
DO  - DOI:10.1002/glia.23751
UR  - https://pub.dzne.de/record/141697
ER  -