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Astrocytes and microglia in acute cerebral injury underlying cerebral palsy associated with preterm birth.

Authors
  • Mallard, Carina1
  • Davidson, Joanne O2
  • Tan, Sidhartha3
  • Green, Colin R4
  • Bennet, Laura2
  • Robertson, Nicola J5
  • Gunn, Alistair Jan2
  • 1 Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. , (Sweden)
  • 2 Department of Physiology, University of Auckland, Auckland, New Zealand. , (New Zealand)
  • 3 Department of Pediatrics, NorthShore University Health System and University of Chicago, Evanston, Illinois.
  • 4 Department of Ophthalmology, University of Auckland, Auckland, New Zealand. , (New Zealand)
  • 5 Institute of Women's Health, University College London, London, UK.
Type
Published Article
Journal
Pediatric Research
Publisher
Springer Nature
Publication Date
Jan 01, 2014
Volume
75
Issue
1-2
Pages
234–240
Identifiers
DOI: 10.1038/pr.2013.188
PMID: 24336433
Source
Medline
License
Unknown

Abstract

Cerebral palsy is one of the most devastating consequences of brain injury around the time of birth, and nearly a third of cases are now associated with premature birth. Compared with term babies, preterm babies have an increased incidence of complications that may increase the risk of disability, such as intraventricular hemorrhage, periventricular leukomalacia, sepsis, and necrotizing enterocolitis. The response to injury is highly dependent on brain maturity, and although cellular vulnerability is well documented, there is now evidence that premyelinating axons are also particularly sensitive to ischemic injury. In this review, we will explore recent evidence highlighting a central role for glia in mediating increased risk of disability in premature infants, including excessive activation of microglia and opening of astrocytic gap junction hemichannels in spreading injury after brain ischemia, in part likely involving release of adenosine triphosphate (ATP) and overactivation of purinergic receptors, particularly in white matter. We propose the hypothesis that inflammation-induced opening of connexin hemichannels is a key regulating event that initiates a vicious circle of excessive ATP release, which in turn propagates activation of purinergic receptors on microglia and astrocytes. This suggests that developing effective neuroprotective strategies for preterm infants requires a detailed understanding of glial responses.

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