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

LORES-ARNAIZ, S.; LOMBARDI, P.; KARADAYIAN, A.G.; ORGAMBIDE, F.; CICERCHIA, D.; BUSTAMANTE, J.

NEUROCHEMICAL RESEARCH

SPRINGER/PLENUM PUBLISHERS

Lugar: New York; Año: 2016 vol. 41 p. 353 - 363

0364-3190

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.