Cited by 125Neonatal and fetal brain pathologyInfant Development and Preterm CareNeurogenesis and neuroplasticity mechanisms

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Disrupted synaptic development in the hypoxic newborn brain

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Curristin, Sheila M., Cao, Anjun, Stewart, William B., Zhang, Heping, Madri, Joseph A., Morrow, Jon S., Ment, Laura R.·2002·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.232568799PMC PMC137784

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Abstract

Infants born prematurely risk significant life-long cognitive disability, representing a major pediatric health crisis. The neuropathology of this cohort is accurately modeled in mice subjected to sublethal postnatal hypoxia. Massively parallel transcriptome analysis using cDNA microchips (9,262 genes), combined with immunohistochemical and protein assays, reveals that sublethal hypoxia accentuates genes subserving presynaptic function, and it suppresses genes involved with synaptic maturation, postsynaptic function, and neurotransmission. Other significantly affected pathways include those involved with glial maturation, vasculogenesis, and components of the cortical and microtubular cytoskeleton. These patterns reveal a global dysynchrony in the maturation programs of the hypoxic developing brain, and offer insights into the vulnerabilities of processes that guide early postnatal cerebral maturation.

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Authors: Curristin, S. M., Cao, A., Stewart, W. B., Zhang, H., Madri, J. A., Morrow, J. S., & Ment, L. R.
Affiliations: Yale University (US)
Departments of Pathology, Epidemiology and Public Health, Surgery, Pediatrics, and Neurology, Yale University School of Medicine, New Haven, CT 06510
ORCID: Madri, Joseph A.
Morrow, Jon S.
Ment, Laura R.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2002-11-15
Volume: 99
Issue: 24
Pages: 15729-15734
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.232568799
PMC: PMC137784
OpenAlex: W2168015911
Cited by: 125
References: 45
Citations by year: 2026: 3 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 9 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 1 · 2013: 6 · 2012: 6
FWCI: 5.71
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5p20ns032578-03, 5r21ns042238-02, 5p01dk038979-05)
National Heart, Lung, and Blood Institute (T32-HL 07778, T32HL007778)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 38979)
National Institute of Neurological Disorders and Stroke (NS-35476, NS-27116, R01NS027116, NS32578, P01NS035476, NS42238)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Infant Development and Preterm Care
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: neonatal brain, synaptic development, preterm infants, cognitive disability, presynaptic function, postsynaptic function, neurotransmission, glial maturation, vasculogenesis, cytoskeleton, transcriptome, mouse model
MeSH terms: Animals, Animals, Newborn, Hypoxia, Atmosphere Exposure Chambers, Brain Damage, Chronic, Cell Differentiation, Hypoxia, Brain, Cytoskeleton, Disease Models, Animal, Lymphokines, Membrane Proteins, Mice, Inbred C57BL, Microtubules, Nerve Tissue Proteins, Synaptic Transmission, Oligodendroglia, Stress, Physiological, Synapses, Transcription Factors, Transcription, Genetic, Endothelial Growth Factors, Apoptosis, DNA, Complementary, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Intercellular Signaling Peptides and Proteins, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Mice, Hypoxia-Inducible Factor 1, alpha Subunit

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Disrupted synaptic development in the hypoxic newborn brain

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