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A(1) adenosine receptors mediate hypoxia-induced ventriculomegaly

By Christopher P. Turner, Meltem Seli, Laura Ment, William Stewart, Henglin Yan, Björn Johansson, Bertil B. Fredholm, Michael Blackburn and Scott A. Rivkees

Abstract

Periventricular leukomalacia is characterized by a reduction in brain matter and secondary ventriculomegaly and is a major cause of developmental delay and cerebral palsy in prematurely born infants. Currently, our understanding of the pathogenesis of this condition is limited. In animal models, features of periventricular leukomalacia can be induced by hypoxia and activation of A(1) adenosine receptors (A(1)ARs). Using mice that are deficient in the A(1)AR gene (A(1)AR–/–), we show that A(1)ARs play a prominent role in the development of hypoxia-induced ventriculomegaly in neonates. Supporting a role for adenosine in the pathogenesis of developmental brain injury, ventriculomegaly was also observed in mice lacking the enzyme adenosine deaminase, which degrades adenosine. Thus, adenosine acting on A(1)ARs appears to mediate hypoxia-induced brain injury ventriculomegaly during early postnatal development

Topics: Biological Sciences
Publisher: National Academy of Sciences
Year: 2003
DOI identifier: 10.1073/pnas.1931975100
OAI identifier: oai:pubmedcentral.nih.gov:208824
Provided by: PubMed Central
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