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L-trans-pyrrolidine-2,4-dicarboxylate and cis-1-aminocyclobutane-1,3-dicarboxylate behave as transportable, competitive inhibitors of the high-affinity glutamate transporters.
TLDR
Results support an action of L-trans-PDC and cis-ACBD consistent with that of being competitive substrates rather than non-transportable blockers of the plasma membrane L-glutamate uptake system. Expand
Synaptosomal plasma membrane transport of excitatory sulphur amino acid transmitter candidates: Kinetic characterisation and analysis of carrier specificity
TLDR
The transport kinetics of the excitatory sulphur‐containing amino acid (SAA) transmitter candidates and their plasma membrane carrier specificity were studied to suggest a common synaptosomal plasma membrane transport system with L‐glutamate, L‐aspartate, and D‐ aspartate. Expand
Differential Changes in the Content of Amino Acid Neurotransmitters in Discrete Regions of the Rat Brain Prior to the Onset and During the Course of Homocysteine‐Induced Seizures
TLDR
Changes in amino acid concentrations were investigated in selected regions of rat brain prior to the onset and during the course of epileptiform seizures induced by l‐homocysteine, with the hippocampus exhibiting a dramatic increase after seizure onset. Expand
A Prototypic Intracellular Calcium Antagonist, TMB‐8, Protects Cultured Cerebellar Granule Cells Against the Delayed, Calcium‐Dependent Component of Glutamate Neurotoxicity
TLDR
It is suggested that Ca2+ release from a TMB‐8‐sensitive intracellular store may be a necessary step in the onset of glutamate‐induced excitotoxicity in granule cells. Expand
Inhibition by excitatory sulphur amino acids of the high-affinityl-glutamate transporter in synaptosomes and in primary cultures of cortical astrocytes and cerebellar neurons
TLDR
Computer-assisted molecular modelling studies, in which volume contour maps of the sulphur compounds were superimposed on those ofd-aspartate andl-glutamate, demonstrated an order of inhibitory potency which was in agreement with that obtained quantitatively by in vitro kinetic studies. Expand
Sulphur-containing excitatory amino acid-evoked Ca2+-independent release of d-[3H]aspartate from cultured cerebellar granule cells: The role of glutamate receptor activation coupled to reversal of
TLDR
Findings are consistent with a mechanism for the Ca(2+)-independent release of D-[3H]aspartate that is mediated predominantly by activation of excitatory amino acid receptors resulting in a reversal of the high-affinity dicarboxylic amino acid transport system. Expand
Simultaneous measurement by HPLC of the excitatory amino acid transmitter candidates homocysteate and homocysteine sulphinate supports a predominant astrocytic localisation
TLDR
Findings indicate a predominant localisation of HCA and HCSA in astrocytes which, at least in culture, appear to possess the metabolic machinery necessary for synthesising and storing these amino acids without any neuronal influence. Expand
Calcium influx via L‐type voltage‐gated channels mediates the delayed, elevated increases in steady‐state c‐fos mRNA levels in cerebellar granule cells exposed to excitotoxic levels of glutamate
TLDR
The results support the notion that the appearance of a delayed but elevated increase in steady‐state c‐fos mRNA levels following exposure to excitotoxic doses of Glu is mediated specifically by calcium influx via L‐type voltage‐gated channels. Expand
Preliminary evaluation of an in vitro test for assessment of excitotoxicity by measurement of early gene (c-fos mRNA) levels.
TLDR
The results of this study support the proposal that the c-fos mRNA time-ratio test is a specific biomarker of excitotoxicity and has the potential for application in screening newly-designed EAA receptor antagonists in the search for clinically relevant drugs to treat a variety of neuropathologies. Expand
Stimulation of γ‐[3H]Aminobutyric Acid Release from Cultured Mouse Cerebral Cortex Neurons by Sulphur‐Containing Excitatory Amino Acid Transmitter Candidates: Receptor Activation Mediates Two
TLDR
SAA‐stimulated release of [3H] GABA was shown to comprise two distinct components, calcium‐dependent and calcium‐independent, which occur after activation of N‐methyl‐B‐aspartate (NMDA) and non‐NMDA receptors, consistent with a receptor‐mediated, depolarization‐induced reversal of the GABA carrier. Expand
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