251. Postnatal development of the complexes of the electron transport chain in synaptic mitochondria from rat brain.
- Author
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Almeida A, Brooks KJ, Sammut I, Keelan J, Davey GP, Clark JB, and Bates TE
- Subjects
- Acetylcholinesterase metabolism, Animals, Brain metabolism, Brain ultrastructure, Citrate (si)-Synthase metabolism, Electron Transport physiology, Electron Transport Complex II, Electron Transport Complex III metabolism, Electron Transport Complex IV metabolism, Female, In Vitro Techniques, Male, Mitochondria enzymology, Multienzyme Complexes metabolism, NAD metabolism, NAD(P)H Dehydrogenase (Quinone) metabolism, Nerve Tissue Proteins metabolism, Oxidation-Reduction, Oxidoreductases metabolism, Proton-Translocating ATPases metabolism, Rats, Rats, Wistar, Succinate Dehydrogenase metabolism, Synapses enzymology, Synaptosomes enzymology, Brain growth & development, Mitochondria metabolism, Mitochondrial Proton-Translocating ATPases, Synapses metabolism, Synaptosomes metabolism
- Abstract
The postnatal development of the complexes of the electron transport chain in mitochondria isolated from rat brain synaptosomes was investigated. Synaptosomal brain mitochondria were isolated from rats aged 10-60 days, and the activities of mitochondrial complex I, complex II-III, complex IV and complex V were measured. There was a significant increase in the activity of II-III from day 10 to day 15 and complex IV from day 10 to day 21, thereafter the activities of complexes I-III and IV did not change significantly. The activity of complex I did not change significantly during the period 10-60 days post partum. In synaptic mitochondria, complex V activity was higher than in non-synaptic mitochondria, whereas the activity of complex I was lower than in non-synaptic mitochondria. These data show that the complexes of the respiratory chain within synaptic mitochondria have activities different from those of non-synaptic mitochondria and may have major implications for the relative susceptibility of mitochondria in different brain cell types to neurotoxins such as MPP+, hypoxic/ischaemic damage and oxidative stress.
- Published
- 1995
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