Hypoxic-ischemic insult decreases glutamate uptake by hippocampal slices from neonatal rats: Prevention by guanosine

Brain injury secondary to hypoxic-ischemic disease is the predominant form of damage encountered in the perinatal period. The impact of neonatal hypoxia-ischemia (HI) in 7-day-old pups on the high-affinity [ 3H] glutamate uptake into hippocampal slices at different times after insult was examined. I...

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Veröffentlicht in:Experimental neurology 2005-10, Vol.195 (2), p.400-406
Hauptverfasser: Moretto, M.B., Arteni, N.S., Lavinsky, D., Netto, C.A., Rocha, J.B.T., Souza, D.O., Wofchuk, S.
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Sprache:eng
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Zusammenfassung:Brain injury secondary to hypoxic-ischemic disease is the predominant form of damage encountered in the perinatal period. The impact of neonatal hypoxia-ischemia (HI) in 7-day-old pups on the high-affinity [ 3H] glutamate uptake into hippocampal slices at different times after insult was examined. Immediately following, and 1 day after the insult there was no effect. But at 3 to 5 days after the HI insult, glutamate uptake into the hippocampus was markedly reduced; however, after 30 or 60 days the glutamate uptake into hippocampal slices returned to control levels. Also, this study demonstrated the effect of the nucleoside guanosine (Guo) on the [ 3H] glutamate uptake in neonatal HI injury, maintaining the [ 3H] glutamate uptake at control levels when injected before and after insult HI. We conclude that neonatal HI influences glutamate uptake a few days following insult, and that guanosine prevents this action.
ISSN:0014-4886
1090-2430
DOI:10.1016/j.expneurol.2005.06.005