Acidosis reduces NMDA receptor activation, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures.
Brain Res
; 506(2): 339-42, 1990 Jan 08.
Article
en En
| MEDLINE
| ID: mdl-1967968
ABSTRACT
The acidosis which accompanies cerebral ischemia in vivo has been thought to contribute to subsequent neuronal injury. However, recent electrophysiological recordings from hippocampal neurons suggest that H+ can attenuate N-methyl-D-aspartate (NMDA) receptor-mediated cation influx, likely a key event in the pathogenesis of ischemic neuronal injury. Here we report that moderate extracellular acidosis (pH 6.5) markedly reduced the inward whole cell current induced by NMDA on cultured cortical neurons; at pH 6.1, kainate-induced current was additionally reduced. Furthermore, such acidosis reduced the cortical neuronal injury caused by toxic glutamate exposure, as well as the neuronal degeneration and accumulation of 45Ca2+ induced by combined oxygen and glucose deprivation. These findings raise the possibility that moderate acidosis may decrease cortical neuronal vulnerability to ischemic damage.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Acidosis
/
Hipoxia de la Célula
/
Corteza Cerebral
/
Receptores de Neurotransmisores
/
Glucosa
/
Glutamatos
Límite:
Animals
Idioma:
En
Revista:
Brain Res
Año:
1990
Tipo del documento:
Article