TY - JOUR
TI - Effects of dexamethasone on K+-evoked glutamate release from rat hippocampal slices
AU - Ioannou, N.
AU - Liapi, C.
AU - Sekeris, C.E.
AU - Palaiologos, G.
JO - Neurochemical Research
PY - 2003
VL - 28
TODO - 6
SP - 875-881
PB - 
SN - 0364-3190, 1573-6903
TODO - 10.1023/A:1023271325728
TODO - 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
TODO - 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.
ER -