EARLY SODIUM ELEVATIONS INDUCED BY COMBINED OXYGEN AND GLUCOSE DEPRIVATION IN PYRAMIDAL CORTICAL-NEURONS

We investigated the effects of oxygen (O-2)/glucose deprivation on int racellular sodium concentration ([Na+](i)) of cortical pyramidal cells in a slice preparation of rat frontal cortex. Intracellular recording s were combined with microfluorometric measurements of [Na+](i) using the Na+-sensitive dye sodium-binding benzofuran isophthalate (SBFI), D eprivation 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 mem brane hyperpolarization. Neither tetrodotoxin, a combination of ionotr opic and metabotropic glutamate receptor antagonists (D-amino-phosphon ovalerate, 6-cyano-7-nitroquinoxaline-2,3-dione plus S-methyl-4-carbox yphenylglycine) nor bepridil, an inhibitor of the Na+/Ca2+-exchanger, affected these responses to O-2/glucose. The present results demonstra te 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+/Ca2+-exchanger.