Extracellular sodium concentration has diverse effects on the hypoxia-induced increase in intracellular Ca 2+ in rat hippocampal slices

Abstract

The intracellular free Ca 2+ concentration ([Ca 2+] i) in the CA1 pyramidal cell layer was measured using fura-2-loaded hippocampal slices prepared from adult rats. Hypoxia (oxygen-glucose deprivation) elicited a gradual increase in [Ca 2+] i in normal Krebs solution. With a high extracellular sodium concentration ([Na +] o), the hypoxia-induced response was attenuated, its onset-latency was longer and the time constant of its decay phase was shorter than in controls. In contrast, hypoxia in low [Na +] o elicited a significantly enhanced response with a short onset-latency and delayed decay phase. This exaggerated response to hypoxia in low [Na +] o was reversed by pre-incubation of the slice in low [Na +] o prior to the hypoxic insult. Some possible mechanisms and the functional significance of the observed effects of [Na +] o on the hypoxia-induced increase in [Ca 2+] i are discussed, with particular emphasis on the putative participation of the glutamate transporter and the sodium-calcium exchanger in hypoxia-induced neuronal injury.