Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses

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 w...

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Bibliographic Details
Published in:	Molecular neurobiology Vol. 55; no. 11; pp. 8668 - 8679
Main Authors:	Lima, Jean Pierre Mendes, Rayêe, Danielle, Silva-Rodrigues, Thaia, Pereira, Paula Ribeiro Paes, Mendonca, Ana Paula Miranda, Rodrigues-Ferreira, Clara, Szczupak, Diego, Fonseca, Anna, Oliveira, Marcus F., Lima, Flavia Regina Souza, Lent, Roberto, Galina, Antonio, Uziel, Daniela
Format:	Journal Article
Language:	English
Published:	New York Springer US 01-11-2018 Springer Nature B.V
Subjects:	Animals Animals, Newborn Asphyxia Asphyxia - blood Asphyxia - pathology Astrocytes Astrocytes - metabolism Astrocytes - pathology Biomedical and Life Sciences Biomedicine Blood-brain barrier Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology Brain Brain - growth & development Brain - metabolism Brain - pathology Brain injury Calcium Calcium buffering Calcium permeability Cell Biology Cell Hypoxia Cell Respiration Cells, Cultured Cellular biology Citrate (si)-Synthase - metabolism Cortex Energy Metabolism Female Fetuses Hypoxia Lactates - blood Membrane permeability Membrane Potential, Mitochondrial Mitochondria Mitochondria - metabolism Mitochondria - pathology Mitochondrial Membranes - metabolism Neonates Neurobiology Neurodegenerative diseases Neurology Neurons Neurons - metabolism Neurons - pathology Neurosciences Organ Size Oxygen consumption Perinatal care Permeability Rats, Wistar Suffocation Survival Analysis Development Mitochondrial metabolism Perinatal asphyxia Cerebral cortex
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0893-7648 1559-1182
DOI:	10.1007/s12035-018-1019-7