Effect of repeated hyperammonemia on Na(+)-dependent binding of glutamate in rat cortical and hippocampal synaptic membranes
Jazyk angličtina Země Irsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
7901815
DOI
10.1016/0304-3940(93)90625-u
PII: 0304-3940(93)90625-U
Knihovny.cz E-zdroje
- MeSH
- amoniak krev MeSH
- glutamátové receptory účinky léků metabolismus MeSH
- glutamáty metabolismus MeSH
- hipokampus metabolismus ultrastruktura MeSH
- kinetika MeSH
- krysa rodu Rattus MeSH
- kyselina glutamová MeSH
- mozek - chemie fyziologie MeSH
- mozková kůra metabolismus ultrastruktura MeSH
- sodík fyziologie MeSH
- stárnutí metabolismus MeSH
- synaptické membrány metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- amoniak MeSH
- glutamátové receptory MeSH
- glutamáty MeSH
- kyselina glutamová MeSH
- sodík MeSH
Na(+)-dependent binding of L-glutamate in cortical and hippocampal synaptic membranes from hyperammonemic rats was compared to corresponding data in the controls. In hippocampal membranes, repeated hyperammonemia resulted in a 13% and 18% decrease in binding in 20-day-old and 50-day-old rats, respectively. The decrease was statistically significant (P < 0.05) in the older animals and Scatchard analysis revealed a 19% reduction in the number of binding sites without any changes in the affinity. Within the hippocampal formation, the binding in the dentate gyrus was the most sensitive to hyperammonemia where a 21% decrease was found (P < 0.01), whilst the decline of binding in CA1 and CA3 areas of the hippocampus proper was not significant. The results support the idea that excessive accumulation of extracellular glutamate during hyperammonemia is a consequence not only of its increased release, but also of the blocking of Na(+)-dependent binding of glutamate to specific uptake sites.
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