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Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15729-34. Epub 2002 Nov 15.

Disrupted synaptic development in the hypoxic newborn brain.

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1
Department of Pathology, Yale University School of Medicine, New Haven, CT 06510, USA.

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.

PMID:
12438650
PMCID:
PMC137784
DOI:
10.1073/pnas.232568799
[Indexed for MEDLINE]
Free PMC Article

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