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  • Title: Stimulation of [3H]gamma-aminobutyric acid release by calcium chelators in synaptosomes.
    Author: Arias C, Sitges M, Tapia R.
    Journal: J Neurochem; 1984 Jun; 42(6):1507-14. PubMed ID: 6144725.
    Abstract:
    The effect of EGTA on the release of labeled gamma-aminobutyric acid (GABA), glutamate, acetylcholine, and dopamine was studied in superfused synaptosomes from mouse brain. In the absence of both Ca2+ and Mg2+, EGTA and also EDTA at 50 microM or higher concentrations induced a 2.5-5-fold stimulation of [3H]GABA release, similar to that produced by potassium depolarization, whereas only a slight effect, or no effect at all, was observed on the release of the other transmitters studied. The GABA-releasing action of EGTA was practically abolished in the presence of Mg2+. In contrast, the effect of EDTA was also observed when the medium contained Mg2+. Studies on the ionic dependence showed that the stimulation of GABA release by EGTA was abolished in a Na+-free medium. Li+ did not substitute Na+ for the EGTA effect, which was also independent of chloride. This Na+ dependence does not seem to involve voltage-sensitive channels, since tetrodotoxin did not affect the GABA-releasing action of EGTA, whereas in parallel superfusion chambers it blocked over 80% the stimulation of GABA release by veratridine. In contrast, two calcium channel blockers in synaptosomes, La3+ and the cationic dye ruthenium red, greatly inhibited the GABA-releasing effect of EGTA. L-2,4-Diaminobutyric acid, an inhibitor of the Na+-dependent GABA carrier, did not affect the releasing action of EGTA, whereas in a parallel experiment this drug inhibited by more than 90% the exchange of labeled GABA with unlabeled GABA.(ABSTRACT TRUNCATED AT 250 WORDS)
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