| First Author | Lobão-Soares B | Year | 2005 |
| Journal | Neurosci Lett | Volume | 375 |
| Issue | 3 | Pages | 203-6 |
| PubMed ID | 15694261 | Mgi Jnum | J:104877 |
| Mgi Id | MGI:3612942 | Doi | 10.1016/j.neulet.2004.11.012 |
| Citation | Lobao-Soares B, et al. (2005) Normal brain mitochondrial respiration in adult mice lacking cellular prion protein. Neurosci Lett 375(3):203-6 |
| abstractText | 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. |
