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Relation of exocytotic release of gamma-aminobutyric acid to calcium entry through calcium channels or by reversal of the sodium/calcium exchanger in synaptosomes



Relation of exocytotic release of gamma-aminobutyric acid to calcium entry through calcium channels or by reversal of the sodium/calcium exchanger in synaptosomes



Pfluegers Archiv European Journal of Physiology 423(3-4): 314-323



The specific inhibitor of the gamma-aminobutyric acid (GABA) carrier, NNC-711, (1-((2-diphenylmethylene) amino)oxyethyl)-1, 2, 5, 6-tetrahydro-3-pyridine-carboxylic acid hydrochloride, blocks the Ca-2+-independent release of (3H)GABA from rat brain synaptosomes induced by 50 mM K+ depolarization. Thus, in the presence of this inhibitor, it was possible to study the Ca-2+-dependent release of (3H)GABA in the total absence of carrier-mediated release. Reversal of the Na+/Ca-2+ exchanger was used to increase the intracellular free Ca-2+ concentration ((Ca-2+)-i) to test whether an increase in (Ca-2+)-i alone is sufficient to induce exocytosis in the absence of depolarization. We found that the (Ca-2+)-i may rise to values above 400 nM, as a result of Na+/Ca-2+ exchange, without inducing release of (3H)GABA, but subsequent K+ depolarization immediately induced (3H)GABA release. Thus, a rise of only a few nanomolar Ca-2+ in the cytoplasm induced by 50 mM K+ depolarization, after loading the synaptosomes with Ca-2+ by Na+/Ca-2+ exchange, induced exocytotic (3H)GABA release, whereas the rise in cytoplasmic (Ca-2+) caused by reversal of the Na+/Ca-2+ exchanger was insufficient to induce exocytosis, although the value for (Ca-2+)-i attained was higher than that required for exocytosis induced by K+ depolarization. The voltage-dependent Ca-2+ entry due to K+ depolarization, after maximal Ca-2+ loading of the synaptosomes by Na+/Ca-2+ exchange, and the consequent (3H)GABA release could be blocked by 50 mu-M verapamil. Although preloading the synaptosomes with Ca-2+ by Na+/Ca-2+ exchange did not cause (3H)GABA release under any conditions studied, the rise in cytoplasmic (Ca-2+) due to Na+/Ca-2+ exchange increased the sensitivity to external Ca-2+ of the exocytotic release of (3H)GABA induced by subsequent K+ depolarization. Thus, our results show that the vesicular release of (3H)GABA is rather insensitive to bulk cytoplasmic (Ca-2+) and are compatible with the view that GABA exocytosis is triggered very effectively by Ca-2+ entry through Ca-2+ channels near the active zones.

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