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Cerebral Cortex Advance Access published online on January 17, 2008
Cerebral Cortex, doi:10.1093/cercor/bhm247
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Activation of DOR Attenuates Anoxic K+ Derangement via Inhibition of Na+ Entry in Mouse Cortex

Dongman Chao1, Alia Bazzy-Asaad1, Gianfranco Balboni2,3, Severo Salvadori3 and Ying Xia1

1 Department of Pediatrics, Section of Respiratory Medicine, Yale University School of Medicine, New Haven, CT 06520, USA, 2 Department of Toxicology, University of Cagliari, I-09124 Cagliari, Italy, 3 Department of Pharmaceutical Sciences and Biotechnology Center, University of Ferrara, I-44100 Ferrara, Italy

Address correspondence to Ying Xia, MD, PhD, Yale University School of Medicine, Department of Pediatrics, 333 Cedar Street, LMP 3107, New Haven, CT 06520, USA. Email: ying.xia{at}yale.edu.

We have recently found that in the mouse cortex, activation of {delta}-opioid receptor (DOR) attenuates the disruption of K+ homeostasis induced by hypoxia or oxygen–glucose deprivation. This novel observation suggests that DOR may protect neurons from hypoxic/ischemic insults via the regulation of K+ homeostasis because the disruption of K+ homeostasis plays a critical role in neuronal injury under hypoxic/ischemic stress. The present study was performed to explore the ionic mechanism underlying the DOR-induced neuroprotection. Because anoxia causes Na+ influx and thus stimulates K+ leakage, we investigated whether DOR protects the cortex from anoxic K+ derangement by targeting the Na+-based K+ leakage. By using K+-sensitive microelectrodes in mouse cortical slices, we showed that 1) lowering Na+ concentration and substituting with impermeable N-methyl-D-glucamine caused a concentration-dependent attenuation of anoxic K+ derangement; 2) lowering Na+ concentration by substituting with permeable Li+ tended to potentiate the anoxic K+ derangement; and 3) the DOR-induced protection against the anoxic K+ responses was largely abolished by low-Na+ perfusion irrespective of the substituted cation. We conclude that external Na+ concentration greatly influences anoxic K+ derangement and that DOR activation likely attenuates anoxic K+ derangement induced by the Na+-activated mechanisms in the cortex.

Key Words: anoxia • cortex • {delta}-opioid receptor • K+ homeostasis • Na+ influx • neuroprotection


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