Mendes 2018 Mol Neurobiol
|Mendes Lima JP, Rayêe D, Silva-Rodrigues T, Ribeiro Paes Pereira P, Mendonca APM, Rodrigues-Ferreira C, Szczupak D, Fonseca A, Oliveira MF, Souza Lima FR, Lent R, Galina A, Uziel D (2018) Perinatal asphyxia and brain development: mitochondrial damage without anatomical or cellular losses. Mol Neurobiol doi.org/10.1007/s12035-018-1019-7.|
Mendes Lima JP, Rayee D, Silva-Rodrigues T, Ribeiro Paes Pereira P, Mendonca APM, Rodrigues-Ferreira C, Szczupak D, Fonseca A, Oliveira MF, Souza Lima FR, Lent R, Galina A, Uziel D (2018) Mol Neurobiol
Abstract: Perinatal asphyxia remains a significant cause of neonatal mortality and is associated with long-term neurodegenerative disorders. In the present study, we evaluated cellular and subcellular damages to brain development in a model of mild perinatal asphyxia. Survival rate in the experimental group was 67%. One hour after the insult, intraperitoneally injected Evans blue could be detected in the fetuses’ brains, indicating disruption of the blood-brain barrier. Although brain mass and absolute cell numbers (neurons and non-neurons) were not reduced after perinatal asphyxia immediately and in late brain development, subcellular alterations were detected. Cortical oxygen consumption increased immediately after asphyxia, and remained high up to 7 days, returning to normal levels after 14 days. We observed an increased resistance to mitochondrial membrane permeability transition, and calcium buffering capacity in asphyxiated animals from birth to 14 days after the insult. In contrast to ex vivo data, mitochondrial oxygen consumption in primary cell cultures of neurons and astrocytes was not altered after 1% hypoxia. Taken together, our results demonstrate that although newborns were viable and apparently healthy, brain development is subcellularly altered by perinatal asphyxia. Our findings place the neonate brain mitochondria as a potential target for therapeutic protective interventions.
• Keywords: Development, Cerebral cortex, Mitochondrial metabolism, Perinatal asphyxia • Bioblast editor: Kandolf G • O2k-Network Lab: BR Rio de Janeiro Oliveira MF, BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry
Labels: MiParea: Respiration
Stress:Hypoxia Organism: Rat Tissue;cell: Nervous system Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET Pathway: N, NS, ROX HRR: Oxygraph-2k