Limited contribution of astroglial gap junction coupling to buffering of extracellular K+ in CA1 stratum radiatum
Autor: | Steffen Kautzmann, Anne Boehlen, Christian Henneberger, Christian Steinhäuser, Björn Breithausen |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
CA1 Stratum Radiatum Hippocampus Biology Hippocampal formation metabolism [Potassium] 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Extracellular Animals metabolism [Gap Junctions] ddc:610 Rats Wistar metabolism [CA1 Region Hippocampal] Iontophoresis metabolism [Astrocytes] Gap junction metabolism [Synapses] physiology [Membrane Potentials] Rats Coupling (electronics) Microelectrode 030104 developmental biology Neurology metabolism [Neurons] Biophysics 030217 neurology & neurosurgery |
Zdroj: | Glia 68(5), 918-931 (2019). doi:10.1002/glia.23751 |
DOI: | 10.1002/glia.23751 |
Popis: | 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. |
Databáze: | OpenAIRE |
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