25 years of research on global asphyxia in the immature rat brain

M. Barkhuizen, D. L. A. van den Hove, J. S. H. Vles, H. W. M. Steinbusch, B. W. Kramer, A. W. D. Gavilanes*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

34 Citations (Web of Science)

Abstract

Hypoxic-ischemic encephalopathy remains a common cause of brain damage in neonates. Preterm infants have additional complications, as prematurity by itself increases the risk of encephalopathy. Currently, therapy for this subset of asphyxiated infants is limited to supportive care. There is an urgent need for therapies in preterm infants and for representative animal models for preclinical drug development. In 1991, a novel rodent model of global asphyxia in the preterm infant was developed in Sweden. This method was based on the induction of asphyxia during the birth processes itself by submerging pups, still in the uterine horns, in a water bath followed by C-section. This insult occurs at a time-point when the rodent brain maturity resembles the brain of a 22-32 week old human fetus. This model has developed over the past 25 years as an established model of perinatal global asphyxia in the early preterm brain. Here we summarize the knowledge gained on the short- and long-term neuropathological and behavioral effects of asphyxia on the immature central nervous system. (C) 2017 Elsevier Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)166-182
Number of pages17
JournalNeuroscience and Biobehavioral Reviews
Volume75
DOIs
Publication statusPublished - Apr 2017

Keywords

  • Hypoxic-ischemia
  • Encephalopathy
  • Preterm infant
  • Submersion
  • Functional outcome
  • ACUTE PERINATAL ASPHYXIA
  • CESAREAN-SECTION BIRTH
  • LONG-TERM CHANGES
  • HYPOXIC-ISCHEMIC ENCEPHALOPATHY
  • MESSENGER-RNA LEVELS
  • DOPAMINE-MEDIATED BEHAVIOR
  • NONHUMAN PRIMATE MODEL
  • CENTRAL-NERVOUS-SYSTEM
  • NITRIC-OXIDE SYNTHASE
  • IN-VIVO MICRODIALYSIS

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