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Arch Dis Child Fetal Neonatal Ed 89:F190-F192 doi:10.1136/adc.2003.043661
  • Leading article

Injury and repair in developing brain

  1. F M Vaccarino1,
  2. L R Ment2
  1. 1Child Study Center and Department of Neurobiology, Yale University School of Medicine, New Haven, CT, USA
  2. 2Departments of Pediatrics and Neurology, Yale University School of Medicine
  1. Correspondence to:
    Dr Ment
    Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06511, USA; Laura.mentyale.edu

    Animal models show that developmental compensatory mechanisms may promote neural and functional plasticity

    Preterm birth results in considerable disability, yet several reports suggest recovery from injury in developing brain. Developmental compensatory mechanisms may promote neural and functional plasticity, and numerous experimental studies have documented the brain’s ability to engage in regenerative mechanisms to potentially replace injured cells. We review available evidence for recovery from injury in models for the preterm brain and offer hypotheses for targeting time dependent molecular and cellular repair mechanisms that have been recently gathered from animal studies. A better understanding of these adaptive cellular and molecular mechanisms will help clinicians apply knowledge derived from animal models to clinical situations.

    NEWBORN RODENT AS A GOOD MODEL FOR PRETERM BRAIN

    The many neurodevelopmental handicaps that very low birthweight infants experience suggest that preterm birth disrupts the genetically programmed pattern of brain genesis. To develop a clinically relevant model of the effect of preterm birth on developing brain, one must use an animal model that shows that the injury imposed results in neuropathological changes similar to those found in preterm infants and correlate these changes with behavioural outcomes. As in the preterm infant at the end of the second trimester, neuronal generation in the newborn rodent is complete in most regions, axonal and dendritic branching is robust, and synaptogenesis is just beginning.1

    Review of the literature suggests that oxygen deprivation is a major cause of neurodevelopmental disability in preterm infants.2 Although intraventricular haemorrhage, periventricular leucomalacia, and ventriculomegaly are the most commonly recognised and best studied of these circulatory disturbances,2 hypoxia is particularly prevalent among very low birthweight infants and is a common denominator of these abnormalities.3

    Models of both hypoxia-ischaemia and hypoxia have been studied in newborn rodents, and the former results in focal injury to developing brain.4 In contrast, the exposure of …

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