Effects of dexamethasone on K(+)-evoked glutamate release from rat hippocampal slices |
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Authors: | Ioannou Nektaria Liapi Charis Sekeris Constantine E Palaiologos George |
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Institution: | (1) Laboratory of Biological Chemistry, Medical School, University of Athens, Mikras Asias 75, GR 11527 Athens, Greece;(2) Department of Pharmacology, Medical School, University of Athens, Mikras Asias 75, GR 11527 Athens, Greece;(3) Laboratory of Biological Chemistry, Medical School, University of Athens, Mikras Asias 75, GR 11527 Athens, Greece |
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Abstract: | Dexamethasone (DEX) at physiologically elevated (stress) concentration (1 µM) decreased K+-evoked glutamate release from rat hippocampal slices under superfusion in the presence of Ca2+. On the contrary 10 µM DEX increased this K+-evoked glutamate release while 0.1 µM DEX had no effect. The glucocorticoid antagonist for the classic receptor, RU 486, completely reversed the effect of 1 µM DEX. Actinomycin D had no effect. Dexamethasone at 1 µM had no effect on the Ca2+-independent (10 µM Mg2+ replacing 1 mM Ca2+) K+-evoked glutamate release. Dexamethasone at 1 µM or 10 µM had no effect on the phosphate-activated glutaminase—the key enzyme for the biosynthesis of neurotransmitter glutamate. These results suggest that the effect of DEX on K+-evoked glutamate release: (i) depends on its concentration; (ii) is exerted on the Ca2+-dependent (neurotransmitter release), at least at physiological stress concentrations; and (iii) is exerted via the classical receptor but is nongenomic. |
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Keywords: | Glutamate dexamethasone hippocampus phosphate activated glutaminase RU 486 |
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