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SHORT COMUNICATION Early sodium elevations induced by combined oxygen and glucose deprivation in pyramidal cortical neurons
Author(s) -
Pisani Antonio,
Calabresi Paolo,
Tozzi Alessandro,
Bernardi Giorgio,
Knöpfel Thomas
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00398.x
Subject(s) - chemistry , biophysics , glutamate receptor , hyperpolarization (physics) , sodium , depolarization , nmda receptor , kainate receptor , metabotropic receptor , ionotropic effect , metabotropic glutamate receptor , membrane potential , medicine , endocrinology , ampa receptor , receptor , biochemistry , biology , stereochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
We investigated the effects of oxygen (O 2 )/glucose deprivation on intracellular sodium concentration ([Na + ] i ) of cortical pyramidal cells in a slice preparation of rat frontal cortex. Intracellular recordings were combined with microfluorometric measurements of [Na + ] i using the Na + ‐sensitive dye sodium‐binding benzofuran isophthalate (SBFI). Deprivation of O 2 /glucose caused an initial membrane hyperpolarization that was followed by a slowly developing large depolarization. Levels of [Na + ] i started to increase significantly during the phase of membrane hyperpolarization. Neither tetrodotoxin, a combination of ionotropic and metabotropic glutamate receptor antagonists ( d ‐amino‐phosphonovalerate, 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione plus S‐methyl‐4‐carboxyphenylglycine) nor bepridil, an inhibitor of the Na + /Ca 2+ ‐exchanger, affected these responses to O 2 /glucose. The present results demonstrate that, in cortical neurons, O 2 /glucose deprivation induces an early rise in [Na + ] i which cannot be ascribed to the activity of voltage gated Na + ‐channels, glutamate receptors or of the Na + /Ca 2+ ‐exchanger.