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Disrupted synaptic development in the hypoxic newborn brain.


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.

SUBMITTER: Curristin SM 

PROVIDER: S-EPMC137784 | biostudies-literature | 2002 Nov

REPOSITORIES: biostudies-literature

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Disrupted synaptic development in the hypoxic newborn brain.

Curristin Sheila M SM   Cao Anjun A   Stewart William B WB   Zhang Heping H   Madri Joseph A JA   Morrow Jon S JS   Ment Laura R LR  

Proceedings of the National Academy of Sciences of the United States of America 20021115 24


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,  ...[more]

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