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Synaptic glutamate release is modulated by the Na+-driven Cl−/HCO3− exchanger Slc4a8

On the one hand, neuronal activity can cause changes in pH; on the other hand, changes in pH can modulate neuronal activity. Consequently, the pH of the brain is regulated at various levels. Here we show that steady-state pH and acid extrusion were diminished in cultured hippocampal neurons of mice...

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Main Authors: Sinning, Anne (Author) , Liebmann, Lutz (Author) , Kougioumtzes, Alexandra (Author) , Westermann, Martin (Author) , Bruehl, Claus (Author) , Hübner, Christian A. (Author)
Format: Article (Journal)
Language:English
Published: May 18, 2011
In: The journal of neuroscience
Year: 2011, Volume: 31, Issue: 20, Pages: 7300-7311
ISSN:1529-2401
DOI:10.1523/JNEUROSCI.0269-11.2011
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1523/JNEUROSCI.0269-11.2011
Verlag, lizenzpflichtig, Volltext: https://www.jneurosci.org/content/31/20/7300
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Author Notes:Anne Sinning, Lutz Liebmann, Alexandra Kougioumtzes, Martin Westermann, Claus Bruehl, and Christian A. Hübner
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Summary:On the one hand, neuronal activity can cause changes in pH; on the other hand, changes in pH can modulate neuronal activity. Consequently, the pH of the brain is regulated at various levels. Here we show that steady-state pH and acid extrusion were diminished in cultured hippocampal neurons of mice with a targeted disruption of the Na+-driven Cl−/HCO3− exchanger Slc4a8. Because Slc4a8 was found to predominantly localize to presynaptic nerve endings, we hypothesize that Slc4a8 is a key regulator of presynaptic pH. Supporting this hypothesis, spontaneous glutamate release in the CA1 pyramidal layer was reduced but could be rescued by increasing the intracellular pH. The reduced excitability in vitro correlated with an increased seizure threshold in vivo. Together with the altered kinetics of stimulated synaptic vesicle release, these data suggest that Slc4a8 modulates glutamate release in a pH-dependent manner.
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Physical Description:Online Resource
ISSN:1529-2401
DOI:10.1523/JNEUROSCI.0269-11.2011

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