Key result
High KCl concentrations stimulate transient, calcium-dependent oxygen uptake in rat synaptosomes without altering high-energy phosphates.
Why the study?
The mechanisms by which depolarization affects cellular energy production and mitochondrial function in synaptosomes remain unclear.
Depolarization with high KCl stimulates oxygen uptake in rat brain synaptosomes via a calcium-dependent mechanism that appears independent of adenine nucleotides or mitochondrial dehydrogenases.
Caution against clinical translation from rat synaptosomes; leaves open calcium-dependent neuronal energy regulation in vivo.
Addition of high concentrations of KC1 to preparations of rat brain synaptosomes incubated with either glucose or pyruvate caused a transient stimulation of oxygen uptake. This increased respiration was insensitive to 1 mM ouabain and 10 microM ruthenium red but was dependent upon the presence of calcium. With 40 mM KCl in the incubation medium, the levels of high-energy phosphate compounds in the synaptosomes were unaltered, whereas pyridine nucleotides underwent a rapid, albeit small and temporary, oxidation. It is postulated that there is a calcium-dependent mechanism in synaptosomes through which the function of the mitochondrial respiratory chain or of oxidative phosphorylation is stimulated directly without the involvement of either adenine nucleotides or mitochondrial dehydrogenases.
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Erecińska et al. (1991) studied this question. High concentrations of KCl was evaluated on Oxygen uptake. Addition of high concentrations of KCl to rat brain synaptosomes caused a transient, calcium-dependent stimulation of oxygen uptake without altering high-energy phosphate compound levels.
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