Normal brain mitochondrial respiration in adult mice lacking cellular prion protein

• Published in: Neuroscience letters 2005-03, Vol.375 (3), p.203-206
• Main Authors: Lobão-Soares, Bruno, Bianchin, Marino Muxfeldt, Linhares, Marcelo Neves, Carqueja, Cristiane Lima, Tasca, Carla Inês, Souza, Márcia, Marques, Wilson, Brentani, Ricardo, Martins, Vilma R., Sakamoto, Américo C., Carlotti, Carlos Gilberto, Walz, Roger
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Brain - anatomy & histology; Brain - physiology; Brain metabolism; Cell Respiration - physiology; Cellular prion protein; Fundamental and applied biological sciences. Psychology; Membrane Potentials - physiology; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondria - physiology; Mitochondrial respiration; Oxidative stress; PrPC Proteins - deficiency; Respiration; Spectrometry, Fluorescence - methods; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2004.11.012

Cellular prion protein (PrP c) gene ( Prnp) null mice ( Prnp 0/0) 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 Prnp 0/0 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 Prnp 0/0 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 Prnp 0/0 mice.