Extracellular sodium concentration has diverse effects on the hypoxia-induced increase in intracellular Ca2+ in rat hippocampal slices.
The intracellular free Ca2+ concentration ([Ca2+]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 [Ca2+]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 [Ca2+]i are discussed, with particular emphasis on the putative participation of the glutamate transporter and the sodium-calcium exchanger in hypoxia-induced neuronal injury.
Yamaguchi
S
S
Department of Physiology, Dokkyo University School of Medicine, Tochigi, Japan.
Endo
K
K
Kitajima
T
T
Hori
Y
Y
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects*; D000860:Hypoxia / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000494:pharmacology*
D012964:Sodium; D002118:Calcium