Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 100, Issue 20, Pages 11718-11722Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1931975100
Keywords
brain; premature; infant; periventricular leukomalacia
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Funding
- NIAID NIH HHS [R01 AI043572, R01 AI43572] Funding Source: Medline
- NINDS NIH HHS [R01 NS33539, R01 NS033539, P01 NS035476, NS35476] Funding Source: Medline
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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, 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.
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