Early sodium elevations induced by combined oxygen and glucose deprivation in pyramidal cortical neurons.
We investigated the effects of oxygen (O2)/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 O2/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+/Ca2+-exchanger, affected these responses to O2/ glucose. The present results demonstrate that, in cortical neurons, O2/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.
Pisani
A
A
Clinica Neurologica, Dipartimento di Neuroscienze, Università Tor Vergata, Rome, Italy. pisani@uniroma2.it
Calabresi
P
P
Tozzi
A
A
Bernardi
G
G
Knöpfel
T
T
D000818:Animals; D015687:Cell Hypoxia / Q000502:physiology; D002478:Cells, Cultured; D004594:Electrophysiology; D005625:Frontal Lobe / Q000166:cytology / Q000378:metabolism*; D005947:Glucose / Q000172:deficiency*; D015640:Ion Channel Gating; D008564:Membrane Potentials; D008839:Microelectrodes; D017966:Pyramidal Cells / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology
D015222:Sodium Channels; D012964:Sodium; D005947:Glucose