@article{2996352,
    title = "Effects of dexamethasone on K+-evoked glutamate release from rat hippocampal slices",
    author = "Ioannou, N. and Liapi, C. and Sekeris, C.E. and Palaiologos, G.",
    journal = "Neurochemical Research",
    year = "2003",
    volume = "28",
    number = "6",
    pages = "875-881",
    issn = "0364-3190, 1573-6903",
    doi = "10.1023/A:1023271325728",
    keywords = "dactinomycin;  dexamethasone;  glutamic acid;  glutaminase;  mifepristone, amino acid analysis;  animal tissue;  article;  brain depth stimulation;  brain slice;  concentration response;  controlled study;  enzyme activation;  evoked response;  hippocampus;  male;  neurotransmission;  nonhuman;  priority journal;  protein determination;  protein secretion;  rat, Animals;  Calcium;  Dactinomycin;  Dexamethasone;  Glutamic Acid;  Hippocampus;  Kinetics;  Magnesium;  Male;  Mifepristone;  Potassium;  Rats;  Rats, Wistar, Animalia;  Hippocampus hippocampus",
    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 mM Mg2+ replacing 1 mM Ca2+) K+-evoked glutamate release. Dexamethasone at 1 μM or 10 μM and 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."
}