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SHORT COMUNICATION Early sodium elevations induced by combined oxygen and glucose deprivation in pyramidal cortical neurons
Authors:AntonioPisani  PaoloCalabresi  AlessandroTozzi  GiorgioBernardi  ThomasKnöpfel
Institution:;Clinica Neurologica, Dipartimento di Neuroscienze, Università'Tor Vergata', Rome, Italy;IRCCS Ospedale S. Lucia, Rome, Italy;Brain Science Institute, Wako‐shi, Japan
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.
Keywords:electrophysiology  glutamate receptors  ischaemia  Na+
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