Endogenous extracellular glutamate accumulation in rat neocortical cultures by reversal of the transmembrane sodium gradient.
Glutamate excites receptors located on neurons that cause calcium and sodium influx involved in excitatory synaptic transmission. During ischemia, excess glutamate is present in the extracellular space of brain tissue, leading to abnormal levels of calcium influx and eventually to cell death. In mixed neuronal/glial cell cultures we have found that reduction of extracellular sodium concentration below approximately 10 mM causes marked increases in glutamate and aspartate in medium collected 10 min after changing to low sodium. Various data indicate that the accumulated glutamate comes from reversal of normal cellular glutamate uptake, a process also thought to occur during ischemia.
Department of Pharmacology, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Co., Ann Arbor, MI 48105.
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Taylor
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Geer
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Burke
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D016923:Cell Death / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D008564:Membrane Potentials / Q000502:physiology; D009457:Neuroglia / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
D000596:Amino Acids; D005971:Glutamates; D018698:Glutamic Acid; D012964:Sodium