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

Neurochem Res. 2016 Feb;41(1-2):353-63. doi: 10.1007/s11064-015-1817-5. Epub 2016 Jan 28.

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 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.

Keywords: Aging; Cerebral cortex; Depolarization; Non-synaptic mitochondria; Respiration; Synaptosomes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism*
  • Animals
  • Calcium / metabolism
  • Cerebral Cortex / metabolism*
  • Energy Metabolism*
  • Male
  • Membrane Potential, Mitochondrial
  • Mice
  • Mitochondria / metabolism*
  • Synaptosomes / metabolism*

Substances

  • Calcium