These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Effects of glutamate transporter and receptor ligands on neuronal glutamate uptake.
    Author: Boeck CR, Kroth EH, Bronzatto MJ, Jardim FM, Souza DO, Vendite D.
    Journal: Neurosci Res; 2005 Sep; 53(1):77-83. PubMed ID: 16011854.
    Abstract:
    The excitatory amino acids (EAAs) transporters regulate the balance between physiological and pathological signaling over stimulation of the glutamatergic system pathway. The effect of transportable substrates and glutamate (Glu) receptor agonists on Glu uptake in neuronal cells was assessed at different conditions. Cells pre-incubated with Glu, L- or D-aspartate (Asp) and washed presented an inhibition on [(3)H]-Glu uptake and this effect was not mimicked by Glu receptors agonists. The effects of L- and D-Asp were not altered by the presence of N-methyl-d-aspartate (NMDA) receptor antagonists. Thus, the reduction on Glu uptake induced by EAAs is probably linked to the transporter activity. In contrast, the presence of NMDA or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (SR-ACPD) during the pre-incubation and the [(3)H]-Glu uptake assay period increased Glu uptake, whilst kainic acid (KA) had no effect. The NMDA effect was not altered by its antagonists (+/-)-2-amino-5-phosphonopentanoic acid (AP-5) or dizocilpine (MK-801). The SR-ACPD effect was due to the activation of metabotropic Glu receptor, since it was abolished by its antagonist, L(+/-)-2-amino-3-phosphonopropionic acid (L-AP3). Thus, the current studies suggest that the neuronal EAAs transporter is regulated in different manner by transportable substrates and Glu receptor agonists. The possible involvement of this modulation after certain neurotoxicity insults is discussed.
    [Abstract] [Full Text] [Related] [New Search]