Responses to reversible anoxia of intracellular free and bound Ca(2+) in rat cortical slices

Severe anoxia induces destabilisation of intracellular calcium homeostasis in neurones. The mechanism of this effect, and particularly the interrelationship between changes in intracellular concentration of free Ca(2+) ions and the content of the intracellular Ca(2+) stores, during and after anoxia,...

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Bibliographic Details
Published in:Resuscitation 2000-05, Vol.44 (3), p.207-214
Main Authors: Semenov, D G, Samoilov, M O, Zielonka, P, Lazarewicz, J W
Format: Article
Language:English
Subjects:
2-Amino-5-phosphonovalerate - pharmacology
Animals
Calcium - metabolism
Chlortetracycline
Dizocilpine Maleate - pharmacology
Excitatory Amino Acid Antagonists - pharmacology
Fluorescent Dyes
Fura-2
Hypoxia - metabolism
In Vitro Techniques
Intracellular Membranes - metabolism
Olfactory Pathways - metabolism
Oxygen - pharmacology
Rats
Rats, Wistar
Receptors, N-Methyl-D-Aspartate - physiology
Time Factors
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Summary:Severe anoxia induces destabilisation of intracellular calcium homeostasis in neurones. The mechanism of this effect, and particularly the interrelationship between changes in intracellular concentration of free Ca(2+) ions and the content of the intracellular Ca(2+) stores, during and after anoxia, is not clear. We used a superfusion system of rat olfactory cortical slices for the fluorimetric estimation of changes in the intracellular concentration of free Ca(2+) ions and in the level of bound Ca(2+), utilising the fluorescent indicators Fura-2 and chlortetracycline, respectively. It was found that 10-min normoglycaemic anoxia results in simultaneous decrease in bound and increase in free Ca(2+) levels, whereas during 60-min reoxygenation, we detected an increase in both indices. The NMDA receptor antagonists MK-801 and APV attenuated changes in free Ca(2+) level during anoxia and reoxygenation and intensified anoxia-evoked decrease in bound Ca(2+) content, whereas a late post-anoxic increase in bound Ca(2+) was abolished. These data suggest that the influx of extracellular Ca(2+) to neurones via NMDA receptors, plays a critical role in the rise of intracellular free Ca(2+) concentration during and after anoxia. Biphasic changes in bound Ca(2+) content during anoxia and reoxygenation may reflect an anoxia-induced release of Ca(2+) from intracellular stores, followed later by a neuronal calcium overload and refilling of intracellular Ca(2+) binding sites.
ISSN:0300-9572
DOI:10.1016/S0300-9572(00)00136-2