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Postsynaptic fall in intracellular pH induced by GABA-activated bicarbonate conductance
Nature
|November 12, 1987
Summary
Gamma-aminobutyric acid (GABA) triggers a significant efflux of bicarbonate ions through GABA-gated channels, causing a drop in intracellular pH. This GABA-induced acidosis in postsynaptic cells may modulate inhibitory neurotransmission.
Area of Science:
- Neuroscience
- Cell Physiology
Background:
- Synaptic inhibition involves gamma-aminobutyric acid (GABA) acting on chloride channels.
- Recent studies reveal GABA-gated channels are permeable to bicarbonate ions.
- Excitable cells maintain a higher intracellular pH, creating an outward driving force for bicarbonate.
Purpose of the Study:
- To investigate the effect of GABA on intracellular pH (pHi) in crayfish skeletal muscle.
- To determine if GABA influences bicarbonate ion flux and its impact on pHi.
Main Methods:
- Utilized crayfish skeletal muscle preparations.
- Applied GABA in the presence of CO2/bicarbonate.
- Monitored intracellular pH changes and extracellular alkalosis.
- Tested the effect of picrotoxin, a GABA channel blocker.
Main Results:
- GABA application caused a significant decrease in intracellular pH (acidosis).
- A concurrent alkalosis was observed at the extracellular surface.
- These pH changes were dependent on GABA activation and sensitive to picrotoxin.
- Results indicate a GABA-activated bicarbonate conductance.
Conclusions:
- GABA-gated channels facilitate bicarbonate efflux, leading to postsynaptic acidosis.
- This GABA-induced change in pHi can influence neuronal function and inhibitory transmission.
- Bicarbonate permeability of GABA channels plays a crucial role in regulating neuronal excitability.