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Role of Na^+^‐H^+^ and Na^+^‐Ca^2+^ exchange in hypoxia‐related acute astrocyte death by Alexander Bondarenko; Nataliya Svichar; Mitchell Chesler is a Neuroscience article available to read on EtoBox.

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## Abstract Cultured astrocytes do not succumb to hypoxia/zero glucose for up to 24 h, yet astrocyte death following injury can occur within 1 h. It was previously demonstrated that astrocyte loss can occur quickly when the gaseous and interstitial ionic changes of transient brain ischemia are simulated: After a 20–40‐min exposure to hypoxic, acidic, ion‐shifted Ringer (HAIR), most cells died within 30 min after return to normal saline (i.e., “reperfusion”). Astrocyte death required external Ca^2+^ and was blocked by KB‐R7943, an inhibitor of reversed Na^+^‐Ca^2+^ exchange, suggesting that injury was triggered by a rise in [Ca^2+^]~i~. In the present study, we confirmed the elevation of [Ca^2+^]~i~ during reperfusion and studied the role of Na^+^‐Ca^2+^ and Na^+^‐H^+^ exchange in this process. Upon reperfusion, elevation of [Ca^2+^]~i~ was detectable by Fura‐2 and was blocked by KB‐R7943. The low‐affinity Ca^2+^ indicator Fura‐FF indicated a mean [Ca^2+^]~i~ rise to 4.8 ± 0.4 μM. Loading astrocytes with Fura‐2 provided significant protection from injury, presumably due to the high affinity of the dye for Ca^2+^. Injury was prevented by the Na^+^‐H^+^ exchange inhibitors ethyl isopr

Who reads Role of Na^+^‐H^+^ and Na^+^‐Ca^2+^ exchange in hypoxia‐related acute astrocyte death?

Author

Alexander Bondarenko; Nataliya Svichar; Mitchell Chesler

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square (ISSN 0894-1491)

Published

2004

Language

EN

Field

Neuroscience (Life Sciences)