• DOI:10.1038/330163A0
• Corpus ID: 4330077

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}
}

• K. Kaila, J. Voipio
• Published 12 November 1987
• Biology
• Nature

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 −. In the presence of CO2/HCO3 − therefore, activation of GABA-gated channels could give rise to a significant efflux of bicarbonate, leading to a fall in postsynaptic pHi. We have examined the influence of GABA on pHi in crayfish skeletal muscle and we find that in the presence of CO2, GABA induces a dramatic fall in pHi which is coupled to an alkalosis at the extracellular surface. This fall in pHi and the extracellular alkalosis are attributable to a GABA-activated, picrotoxin-sensitive HCO3 −-conductance. In view of the sensitivity of ion channels10 and intracellular ion concentrations5–9 to changes in pHi, a GABA-induced postsynaptic acidosis could prove to be important in the modulation of inhibitory transmission.