Cerebellar granule neurons are more vulnerable to transient transport-mediated glutamate release than to glutamate uptake blockade. Correlation with excitatory amino acids levels


Por: Estrada-Sánchez A.M., Camacho A., Montiel T., Massieu L.

Publicada: 1 ene 2007
Resumen:
The extracellular concentration of glutamate is highly regulated due to its excitotoxic nature. Failure of glutamate uptake or reversed activation of its transporters contributes to neurodegeneration related to some pathological conditions. We have compared the neurotoxicity of the substrate glutamate uptake inhibitor, l-trans-pyrrolidine-2,4-dicarboxylate (PDC), which promotes glutamate release by heteroexchange, with that of DL-threo-beta- benzyloxyaspartate (DL-TBOA), a non-substrate inhibitor, in cerebellar granule cell cultures. PDC substantially increases the extracellular concentration of glutamate during 30 min exposure and causes neuronal death at high concentrations, while DL-TBOA neurotoxicity is only observed after long-term exposure (8-24 h). During mitochondrial inhibition by 3-nitropropionic acid (3-NP), PDC-induced neuronal death is facilitated, but not that of DL-TBOA. In cultures containing a higher population of astrocytes DL-TBOA-induced increase in glutamate levels is more pronounced, but neuronal death is only triggered in the presence of 3-NP. Results suggest that cerebellar granule neurons are more vulnerable to acute transport-mediated glutamate release than to uptake blockade, which correlates with the extracellular excitatory amino acids levels. © 2007 Springer Science+Business Media, LLC.

Filiaciones:
Estrada-Sánchez A.M.:
 Departamento de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, AP 70-253, México, D.F. CP 04510, Mexico

Camacho A.:
 Departamento de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, AP 70-253, México, D.F. CP 04510, Mexico

Montiel T.:
 Departamento de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, AP 70-253, México, D.F. CP 04510, Mexico

Massieu L.:
 Departamento de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, AP 70-253, México, D.F. CP 04510, Mexico
ISSN: 03643190
Editorial
SPRINGER/PLENUM PUBLISHERS, 233 SPRING ST, NEW YORK, NY 10013 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 32 Número: 3
Páginas: 423-432
WOS Id: 000244315200006
ID de PubMed: 17268852