Postsynaptic fall in intracellular pH induced by GABA-activated bicarbonate conductance

@article{Kaila1987PostsynapticFI,
  title={Postsynaptic fall in intracellular pH induced by GABA-activated bicarbonate conductance},
  author={Kai Kaila and Juha Voipio},
  journal={Nature},
  year={1987},
  volume={330},
  pages={163-165}
}
Synaptic inhibition mediated by γ-aminobutyric acid (GABA) is known to involve opening of receptor-gated chloride channels1–3. Recent evidence indicates that these channels also show a significant permeability to the physiologically important bicarbonate anion4. In all the excitable cells studied to date, the intracellular pH (pHi) is higher than would be predicted from a passive distribution of H+ ions5–9, and consequently there is an outwardly directed electrochemical driving force for HCO3… 
Intracellular chloride and calcium transients evoked by gamma-aminobutyric acid and glycine in neurons of the rat inferior colliculus.
TLDR
It is suggested that the activation of GABAA or glycine receptors results in an acute accumulation of Cl- that is enhanced by the depolarization owing to HCO3- efflux, thus shifting E(GABA/gly) to more positive values.
Influence of GABA‐gated bicarbonate conductance on potential, current and intracellular chloride in crayfish muscle fibres.
TLDR
In both the presence and absence of HCO3‐, the GABA‐activated transmembrane flux of Cl‐ showed reversal at the level of the resting potential, which indicates that under steady‐state conditions the Cl‐ equilibrium potential (ECl) is identical to the resting Potential (EHCO3).
Bicarbonate efflux via GABAA receptors depolarizes membrane potential and inhibits two‐pore domain potassium channels of astrocytes in rat hippocampal slices
TLDR
Analysis of gramicidin perforated‐patch recordings from rat hippocampal CA1 astrocytes showed that GABAA‐R‐induced Vm depolarization was ascribed to HCO3− efflux, while a passively distributed Cl− mediated no net flux or influx of Cl− that leads to an unchanged or hyperpolarized Vm.
Anion transport and GABA signaling
TLDR
Current knowledge about the role of some bicarbonate transporters for brain development and brain function is summarized.
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