Limited contribution of astroglial gap junction coupling to buffering of extracellular K+ in CA1 stratum radiatum.

Breithausen, Björn; Steinhäuser, Christian; Boehlen, Anne; Henneberger, Christian; Kautzmann, Steffen

doi:10.1002/glia.23751

Journal Article

DZNE-2020-00028

Limited contribution of astroglial gap junction coupling to buffering of extracellular K+ in CA1 stratum radiatum.

Breithausen, B. ; Kautzmann, S. ; Boehlen, A. ; Steinhäuser, C. ; Henneberger, C. (Last author)DZNE*

2019
Wiley-Liss Bognor Regis [u.a.]

Glia 68(5), 918-931 (2019) [10.1002/glia.23751]

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Please use a persistent id in citations: doi:10.1002/glia.23751

Abstract: 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.

Keyword(s): Animals (MeSH) ; Astrocytes: metabolism (MeSH) ; CA1 Region, Hippocampal: metabolism (MeSH) ; Gap Junctions: metabolism (MeSH) ; Membrane Potentials: physiology (MeSH) ; Neurons: metabolism (MeSH) ; Potassium: metabolism (MeSH) ; Rats (MeSH) ; Rats, Wistar (MeSH) ; Synapses: metabolism (MeSH)