The effect of excess K+ on two different tricarboxylate cycles in rat brain cortex slices
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
6446094
Knihovny.cz E-zdroje
- MeSH
- acetáty metabolismus MeSH
- adenosintrifosfát metabolismus MeSH
- aminokyseliny metabolismus MeSH
- citrátový cyklus účinky léků MeSH
- draslík farmakologie MeSH
- GABA metabolismus MeSH
- glukosa metabolismus MeSH
- glutamáty metabolismus MeSH
- glutamin metabolismus MeSH
- krysa rodu Rattus MeSH
- kyselina asparagová metabolismus MeSH
- mozková kůra metabolismus MeSH
- oxid uhličitý metabolismus MeSH
- spotřeba kyslíku účinky léků MeSH
- techniky in vitro MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- acetáty MeSH
- adenosintrifosfát MeSH
- aminokyseliny MeSH
- draslík MeSH
- GABA MeSH
- glukosa MeSH
- glutamáty MeSH
- glutamin MeSH
- kyselina asparagová MeSH
- oxid uhličitý MeSH
The authors compared, in rat brain cortex slices, the oxidation of labelled glucose and acetate and the conversion of these precursors into amino acids during incubation in control salt-glucose medium and in medium with 47 mM K+, with the aim of determining with which of the two determinable tricarboxylate cycles raised oxygen consumption is associated in the presence of excess K+. Under the experimental conditions it was found that from U-[14C]-glucose more than double the amount of [14C]-CO2 was formed and that the rate of [14C] incorportation into the amino acids was likewise roughly doubled. This is indicative of activation of processes in the tricarboxylate cycle associated with the large glutamate pool. Incorporation from 1-[14C]-acetate into the total amino acids was not affected. Specific activity in glutamate and asparate was more than doubled, while glutamine specific activity fell to less than half. [14C]-CO2 production fell to 65%. This shows that the tricarboxylate cycle associated with the small glutamate pool, which is probably localized in the glia cells, did not participate in raised oxygen consumption in the presence of excess K+.