36 research outputs found
Group I and II metabotropic glutamate receptors alter brain cortical metabolic and glutamate/glutamine cycle activity: a 13C NMR spectroscopy and metabolomic study
Comparative Analysis of 13C-Enriched Metabolites Released in the Medium of Cerebellar and Cortical Astrocytes Incubated with [1-13C]Glucose
Metabolic Effects of Blocking Lactate Transport in Brain Cortical Tissue Slices Using an Inhibitor Specific to MCT1 and MCT2
Effects of glutamate transport substrates and glutamate receptor ligands on the activity of Na+/K+-ATPase in brain tissue in vitro
1. It has been suggested that Na+/K+-ATPase and Na+-dependent glutamate transport (GluT) are tightly linked in brain tissue. In the present study, we have investigated Na+/K +-ATPase activity using Rb+ uptake by 'minislices' (prisms) of the cerebral cortex. This preparation preserves the morphology of neurons, synapses and astrocytes and is known to possess potent GluT that has been well characterized. Uptake of Rb+ was determined by estimating Rb+ in aqueous extracts of the minislices, using atomic absorption spectroscopy. 2. We determined the potencies of several known substrates/inhibitors of GluT, such as L-trans-pyrrolidine-2,4-dicarboxylate (LtPDC), DL-threo-3-benzyloxyaspartic acid, (2S,3S,4R)-2-(carboxycyclopropyl)- glycine (L-CCG III) and L-anti,endo-3,4-methanopyrrolidine dicarboxylic acid, as inhibitors of [3H]-L-glutamate uptake by cortical prisms. In addition, we established the susceptibility of GluT, measured as [ 3H]-L-glutamate uptake in brain cortical prisms, to the inhibition of Na+/K+-ATPase by ouabain. Then, we tested the hypothesis that the Na+/K+-ATPase (measured as Rb+ uptake) can respond to changes in the activity of GluT produced by using GluT substrates as GluT-specific pharmacological tools. 3. The Na+/K +-ATPase inhibitor ouabain completely blocked Rb+ uptake (IC50 = 17 μmol/L), but it also potently inhibited a fraction of GluT (approximately 50% of [3H]-L-glutamate uptake was eliminated; IC50 < 1 μmol/L). 4. None of the most commonly used GluT substrates and inhibitors, such as L-aspartate, D-aspartate, L-CCG III and LtPDC (all at 500 μmol/L), produced any significant changes in Rb+ uptake. 5. The N-methyl-D-aspartate (NMDA) receptor agonists (R,S)-(tetrazol-5-yl)-glycine and NMDA decreased Rb+ uptake in a manner compatible with their known neurotoxic actions. 6. None of the agonists or antagonists for any of the other major classes of glutamate receptors caused significant changes in Rb+ uptake. 7. We conclude that, even if a subpopulation of glutamate transporters in the rat cerebral cortex may be intimately linked to a fraction of Na+/K+-ATPase, it is not possible, under the present experimental conditions, to detect regulation of Na+/K+-ATPase by GluT.Fil: Acosta, Gabriela Beatriz. ININFA; Argentin
A brain uptake study of [1-11C]hexanoate in the mouse: The effect of hypoxia, starvation and substrate competition
Effects of food restriction on expression of place conditioning and biochemical correlates in rat nucleus accumbens
Entry of [(1,2-13C2)acetyl]- l-carnitine in liver tricarboxylic acid cycle and lipogenesis . A study by 13C NMR spectroscopy in conscious, freely moving rats
EFFECTS OF GLUTAMATE TRANSPORT SUBSTRATES AND GLUTAMATE RECEPTOR LIGANDS ON THE ACTIVITY OF Na+/K+-ATPase IN BRAIN TISSUE IN VITRO
Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice
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