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

Abstract

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 decresed by 26 and 33% in sunaptosomes from 17-months old mice, but spare respiratory rate was decreased by 45% in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animales, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non synaptic mitochondrian would not be affectred by calcium overload. UCP2 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.