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Alkaline extracellular pH shifts generated by two transmitter-dependent mechanisms
1Department of Physiology and Biophysics, New York University Medical Center, NY 10016.
Canadian Journal of Physiology and Pharmacology
|January 1, 1992
Summary
Gamma-aminobutyric acid (GABA) causes brain pH changes by affecting bicarbonate ions. Separate mechanisms regulate pH shifts during GABA receptor activation versus excitatory transmission.
Area of Science:
- Neuroscience
- Neurophysiology
- Biochemistry
Background:
- Extracellular pH regulation is crucial for neuronal function.
- Gamma-aminobutyric acid (GABA) is a primary inhibitory neurotransmitter.
- The precise mechanisms of GABA's effect on brain pH remain under investigation.
Purpose of the Study:
- To investigate the impact of GABA on extracellular pH in the turtle cerebellum.
- To differentiate the mechanisms underlying GABA-evoked pH changes from those of excitatory transmission.
Main Methods:
- Utilized double-barrelled pH-sensitive microelectrodes in isolated turtle cerebellum.
- Administered GABA and GABA-A agonists (isoguvacine, muscimol) and antagonists (picrotoxin).
- Manipulated extracellular calcium and bicarbonate concentrations.
Main Results:
- GABA induced an alkaline shift and increased extracellular K+, blocked by picrotoxin.
- GABA-evoked responses persisted without calcium but were abolished in bicarbonate-free media.
- Excitatory transmission caused bicarbonate-independent alkaline shifts, unaffected by picrotoxin.
Conclusions:
- GABA-A receptor activation mediates extracellular alkalinization likely via bicarbonate efflux.
- Excitatory synaptic transmission utilizes a distinct, bicarbonate-independent mechanism for pH regulation.