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The Journal of Neuroscience, December 8, 2004, 24(49):11057-11069; doi:10.1523/JNEUROSCI.2829-04.2004

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Neurobiology of Disease
Sodium Influx Pathways during and after Anoxia in Rat Hippocampal Neurons

Claire Sheldon,¹ Abdoullah Diarra,² Y. May Cheng,¹ and John Church^1,2

Departments of ¹Physiology and ²Anatomy and Cell Biology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3

Mechanisms that contribute to Na⁺ influx during and immediately after 5 min anoxia were investigated in cultured rat hippocampal neurons loaded with the Na⁺-sensitive fluorophore sodium-binding benzofuran isophthalate. During anoxia, an influx of Na⁺ in the face of reduced Na⁺,K⁺-ATPase activity caused a rise in [Na⁺]_i. After the return to normoxia, Na⁺,K⁺-ATPase activity mediated the recovery of [Na⁺]_i despite continued Na⁺ entry. Sodium influx during and after anoxia occurred through multiple pathways and increased the longer neurons were maintained in culture. Under the experimental conditions used, Na⁺ entry during anoxia did not reflect the activation of ionotropic glutamate receptors, TTX- or lidocaine-sensitive Na⁺ channels, plasmalemmal Na⁺/Ca²⁺ exchange, Na⁺/H⁺ exchange, or -dependent mechanisms; rather, contributions were received from a Gd³⁺-sensitive pathway activated by reactive oxygen species and Na⁺/K⁺/2Cl^- cotransport in neurons maintained for 6-10 and 11-14 d in vitro (DIV), respectively. Sodium entry immediately after anoxia was not attributable to the activation of ionotropic glutamate receptors, voltage-activated Na⁺ channels, or Na⁺/K⁺/2Cl^- cotransport; rather, it occurred via Na⁺/Ca²⁺ exchange, Na⁺/H⁺ exchange, and a Gd³⁺-sensitive pathway similar to that observed during anoxia; 11-14 DIV neurons received an additional contribution from an -dependent mechanism(s). The results provide insight into the intrinsic mechanisms that contribute to disturbed internal Na⁺ homeostasis during and immediately after anoxia in rat hippocampal neurons and, in this way, may play a role in the pathogenesis of anoxic or ischemic cell injury.

Key words: anoxia; ischemia; intracellular sodium; Na⁺/K⁺/2Cl^- cotransport; Na⁺/Ca²⁺ exchange; Na⁺/H⁺ exchange; Gd³⁺

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Received July 14, 2004; revised October 30, 2004; accepted November 2, 2004.

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