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

Nature. 1987 Nov 12-18;330(6144):163-5. doi: 10.1038/330163a0.


Synaptic inhibition mediated by gamma-aminobutyric acid (GABA) is known to involve opening of receptor-gated chloride channels. Recent evidence indicates that these channels also show a significant permeability to the physiologically important bicarbonate anion. In all the excitable cells studied to date, the intracellular pH (pHi) is higher than would be predicted from a passive distribution of H+ ions, 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 channels and intracellular ion concentrations to changes in pHi, a GABA-induced postsynaptic acidosis could prove to be important in the modulation of inhibitory transmission.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astacoidea
  • Bicarbonates / metabolism*
  • Bicarbonates / pharmacology
  • Body Fluids / physiology*
  • Cell Membrane / physiology
  • Electric Conductivity
  • Hydrogen-Ion Concentration
  • Intracellular Fluid / physiology*
  • Membrane Potentials / drug effects
  • Muscles / drug effects
  • Muscles / physiology*
  • Synapses / drug effects
  • Synapses / physiology*
  • gamma-Aminobutyric Acid / pharmacology*


  • Bicarbonates
  • gamma-Aminobutyric Acid