Brain cortex mitochondrial bioenergetics in synaptosomes and non-synaptic mitochondria during aging

Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated b...

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Bibliographic Details
Published in:Neurochemical research 2016-02, Vol.41 (1-2), p.353-363
Main Authors: Lores-Arnaiz, Silvia, Lombardi, Paulina, Karadayian, Analía G., Orgambide, Federico, Cicerchia, Daniela, Bustamante, Juanita
Format: Article
Language:English
Subjects:
Aging - metabolism
Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Calcium - metabolism
Cell Biology
Cerebral Cortex - metabolism
Energy Metabolism
Male
Membrane Potential, Mitochondrial
Mice
Mitochondria - metabolism
Neurochemistry
Neurology
Neurosciences
Original Paper
Synaptosomes - metabolism
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Summary:Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated by oxygen consumption, mitochondrial membrane potential and respiratory complexes activity, together with UCP-2 protein expression. Basal respiration and respiration driving proton leak were decreased by 26 and 33 % in synaptosomes from 17-months old mice, but spare respiratory capacity was not modified by aging. Succinate supported state 3 respiratory rate was decreased by 45 % in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animals, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non-synaptic mitochondria would not be affected by calcium overload. UCP-2 was significantly up-regulated in both synaptosomal and submitochondrial membranes from 17-months old mice, compared to young animals. UCP-2 upregulation seems to be a possible mechanism by which mitochondria would be resistant to suffer oxidative damage during aging.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-015-1817-5