Transient acidosis induces delayed neurotoxicity in cultured hippocampal slices

Transient acidosis induces delayed neurotoxicity in cultured hippocampal slices

It remains unknown if tissue acidosis contributes to neuronal loss during cerebral ischemia. We report that brief intracellular acidification (pH 6.62) results in delayed neuronal loss in cultured hippocampal slices. Cell loss was located primarily in stratum pyramidale and the hilus suggesting that...

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Bibliographic Details
Published in:Neuroscience letters Vol. 185; no. 2; pp. 115 - 118
Main Authors: Shen, H., Chan, J., Kass, I.S., Bergolda, P.J.
Format: Journal Article
Language:English
Published: Shannon Elsevier Ireland Ltd 09-02-1995
Elsevier
Subjects:
Acidosis
Animals
BCECF
Biological and medical sciences
Brain Ischemia - pathology
Cell Count
Cells, Cultured
Cerebral ischemia
Hippocampus - pathology
Hydrogen-Ion Concentration
Hypoxia
Intracellular pH
Medical sciences
Neurology
Organotypic
Oxygen
Propidium iodide
Rats
Vascular diseases and vascular malformations of the nervous system
Intracellular pH
Propidium iodide
Cerebral ischemia
Oxygen
Organotypic
BCECF
Nervous system diseases
Rat
Rodentia
Acidification
In vitro
Free radical
Cerebral disorder
Vertebrata
Mammalia
Neuron
Ischemia
Cell death
Animal
Central nervous system disease
pH
Acidosis
Cerebrovascular disease
Hippocampus
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Summary:It remains unknown if tissue acidosis contributes to neuronal loss during cerebral ischemia. We report that brief intracellular acidification (pH 6.62) results in delayed neuronal loss in cultured hippocampal slices. Cell loss was located primarily in stratum pyramidale and the hilus suggesting that neurons were preferentially damaged. Removal of molecular oxygen greatly attenuated cell loss suggesting that generation of reactive oxygen species may underlie acidosis-induced toxicity. These data suggest that acidosis and incomplete anoxia contributes to the delayed neuronal loss in the ischemic penumbra.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0304-3940
1872-7972
DOI:10.1016/0304-3940(94)11238-E