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.

authors

Curristin SM,Cao A,Stewart WB,Zhang H,Madri JA,Morrow JS,Ment LR

doi

10.1073/pnas.232568799

keywords:

subject

Has Abstract

pub_date

2002-11-26 00:00:00

pages

15729-34

issue

24

eissn

0027-8424

issn

1091-6490

pii

232568799

journal_volume

99

pub_type

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