Cortical neurons exposed to glutamate rapidly leak preloaded 51chromium.
The acute toxic effects of excess glutamate exposure on cortical neurons in culture was followed using a novel adaptation of the 51chromium efflux assay. Although the acute, sodium-dependent phase of glutamate neurotoxicity may contribute to several acute disease settings, including sustained seizures and stroke, functional aspects of the phenomenon have not been previously studied. We report here that the earliest morphologic sign of glutamate neurotoxicity, neuronal swelling, is accompanied by a large efflux of complexed 51chromium from preloaded neurons in the first hour after exposure, and that this efflux is detectable as early as 15 min after the onset of glutamate exposure. We suggest that this pathological burst of 51chromium may result from glutamate-induced "leakiness" of neuronal cell membranes.
D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D002860:Chromium Radioisotopes; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
D002860:Chromium Radioisotopes; D005971:Glutamates; D018698:Glutamic Acid