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- W1973358820 abstract "Cellular prion protein (PrP(c)) gene (Prnp) null mice (Prnp0/0) show higher sensitivity to seizures, enhanced brain oxidative stress, and their neurons exhibit higher excitability in vitro. Mitochondrial respiration is a useful parameter for the determination of cellular metabolic rate and it is a major source of reactive oxygen species (ROS). In the present study, we investigated the mitochondrial function of different brain areas of Prnp0/0 adult mice and then compared this to normal control animals. Baseline mitochondrial respiration (stages 3 and 4), respiratory control ratio (RCR) and membrane potential were evaluated in the neocortex, entorhinal cortex, hippocampus, and cerebellum. No differences in these parameters were detected between Prnp0/0 and wild-type mice. Thus, we concluded that baseline mitochondrial respiration might not be directly related with the higher oxidative stress previously observed in brains from Prnp0/0 mice." @default.
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- W1973358820 date "2005-03-01" @default.
- W1973358820 modified "2023-09-25" @default.
- W1973358820 title "Normal brain mitochondrial respiration in adult mice lacking cellular prion protein" @default.
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- W1973358820 doi "https://doi.org/10.1016/j.neulet.2004.11.012" @default.
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