Alkaline extracellular pH shifts generated by two transmitter-dependent mechanisms.

Article date: 1992/1/1

PubMed ID: 1363531

Journal name: Canadian journal of physiology and pharmacology (ISSN: 0008-4212)


Recent studies of the effect of gamma-aminobutyric acid (GABA) on brain extracellular pH are reviewed. Experiments were performed on isolated turtle cerebellum, using double-barrelled pH-sensitive microelectrodes. Superfusion of GABA (1 mM) caused a rapid extracellular alkaline shift accompanied by a rise in extracellular K+. Washout of GABA was often associated with an acid rebound, concomitant with an undershoot of extracellular K+. The GABA-evoked alkaline shift was blocked by picrotoxin and mimicked by the GABA-A agonists isoguvacine and muscimol. The response persisted in the nominal absence of extracellular calcium, but it was reversibly abolished in nominally bicarbonate free media. In contrast, extracellular alkaline shifts evoked by repetitive stimulation of the parallel fibers were amplified in bicarbonate-free media and were insensitive to picrotoxin. These results indicate the existence of separate, transmitter-dependent mechanisms of extracellular alkalinization: (i) a GABA-A receptor mediated process, most likely associated with efflux of bicarbonate ions across GABA-A anion channels and (ii) a bicarbonate-independent process associated with excitatory synaptic transmission.

This document is available from: http://directlinks.cc/files/muscimol/1363531.pdf

Author List: Chesler M, Chen J C

Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.; Review

Substances mentioned in the article: Neurotransmitter Agents; gamma-Aminobutyric Acid;

Mesh terms: Animals; Extracellular Space/drug effects; Hydrogen-Ion Concentration; In Vitro Techniques; Neurotransmitter Agents/physiology; Turtles; gamma-Aminobutyric Acid/pharmacology;

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