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

• Verfasst von: Sinning, Anne [VerfasserIn]
• Verfasst von: Liebmann, Lutz [VerfasserIn]
• Verfasst von: Kougioumtzes, Alexandra [VerfasserIn]
• Verfasst von: Westermann, Martin [VerfasserIn]
• Verfasst von: Bruehl, Claus [VerfasserIn]
• Verfasst von: Hübner, Christian A. [VerfasserIn]
• Titel: Synaptic glutamate release is modulated by the Na+-driven Cl−/HCO3− exchanger Slc4a8
• Verf.angabe: Anne Sinning, Lutz Liebmann, Alexandra Kougioumtzes, Martin Westermann, Claus Bruehl, and Christian A. Hübner
• E-Jahr: 2011
• Jahr: May 18, 2011
• Umfang: 12 S.
• Fussnoten: Gesehen am 17.10.2022 ; Im Titel sind das Pluszeichen und die Minuszeichen hochgestellt ; Im Titel ist die Zahl 3 tiefgestellt
• Titel Quelle: Enthalten in: The journal of neuroscience
• Ort Quelle: Washington, DC : Soc., 1981
• Jahr Quelle: 2011
• Band/Heft Quelle: 31(2011), 20, Seite 7300-7311
• ISSN Quelle: 1529-2401
• DOI: doi:10.1523/JNEUROSCI.0269-11.2011
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1818990393

Abstract

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.