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Cited by 367

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Acidosis reduces NMDA receptor activation, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures

Open access
Giffard, Rona G., Monyer, Hannelore, Christine, Chadwick W., Choi, Dennis W.·1990·Brain Research
DOI 10.1016/0006-8993(90)91276-m
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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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Metadata

Authors
Giffard, R. G., Monyer, H., Christine, C. W., & Choi, D. W.
Venue
Brain Research
Publisher
Elsevier BV
Published
1990-01
Volume
506
Issue
2
Pages
339-342
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/0006-8993(90)91276-m
OpenAlex
W2033275198
Cited by
367
References
1
FWCI
9.85
Type
journal article
Language
en
Open access
hybrid

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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