Abstract
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.
Original language | English |
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Pages (from-to) | 3572-3574 |
Number of pages | 3 |
Journal | European Journal of Neuroscience |
Volume | 10 |
Issue number | 11 |
DOIs | |
Publication status | Published - 1998 |
Keywords
- Electrophysiology
- Glutamate receptors
- Ischaemia
- Na/Ca-exchanger
- Optical recordings
- Sodium channels
ASJC Scopus subject areas
- Neuroscience(all)