Effects of Postdecapitative Ischemia on Mitochondrial Respiration in Brain Tissue Homogenates

Neil R. Sims, Janet M. Finegan, John P. Blass

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)

Abstract

Abstract: Mitochondria isolated from ischemic brain characteristically show changes in respiratory function. As conventional procedures for mitochondrial isolation yield a subpopulation of the total population and require extensive manipulation, it is unclear to what extent these changes are representative of mitochondria in the unfractionated tissue. We previously showed that the oxygen uptake by unfractionated forebrain homogenates, measured under two different sets of incubation conditions, provided information on some aspects of the respiratory activity of both the free and synaptosomal pools of mitochondria. Forebrain homogenates from animals subjected to 30 min of postdecapitative ischemia exhibited large reductions in oxygen uptake rates measured in a high K+ (mitochondrial) buffer in the presence of either ADP (44% of control values) or an uncoupling agent (45% of control values). These reductions in respiratory activity were comparable to alterations observed under the same conditions for mitochondria isolated from the ischemic brains. Similar alterations were seen in homogenates from three subregions: neocortex, hippocampus, and striatum. In a physiological buffer, in which oxygen uptake by homogenates largely resulted from activity of mitochondria within synaptosomes, there was little or no change in basal glucose‐supported rates (79–96% of control values) and small reductions in maximal rates (63–81% of control values) measured in the presence of an uncoupling agent. These results suggest that alterations of respiratory function seen in isolated free mitochondria provide appropriate estimates of the dysfunction in the total free mitochondrial pool but that synaptosomal mitochondria may be less affected. Measurements of respiratory function of isolated synaptosomes from ischemic tissue provided further support for the relative preservation of synaptosomal mitochondria during ischemic insult.

Original languageEnglish
Pages (from-to)506-511
Number of pages6
JournalJournal of Neurochemistry
Volume47
Issue number2
DOIs
Publication statusPublished - Aug 1986
Externally publishedYes

Keywords

  • IschemiA
  • MitochondriA
  • Oxygen uptake
  • Synaptosomes

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