title: The effects of vascular intrauterine growth retardation on cortical astrocytes.
abstract: OBJECTIVE
  We sought to determine the pathogenesis of neurodevelopmental impairments in survivors of intrauterine growth retardation (IUGR).
  
  
  METHODS
  We used an experimental rabbit vascular IUGR model. We ligated 25% of uteroplacental vessels (partial ischemia) of one-half of the fetuses on day 25 at the end of the third trimester. We then determined hemispheral DNA and protein levels, and used glial fibrillary acidic protein (GFAP) staining to count the labeled astrocytes at the superficial cortical layers.
  
  
  RESULTS
  Ischemic fetuses were significantly smaller than control fetuses and presented a disproportionately small body and a relatively larger head compared with the normal body/head ratio, confirming the study model as that of asymmetric IUGR. Hemispheral DNA was unchanged in IUGR fetuses, but they had decreased brain weight, hemispheral protein content, and a reduced number of mature (GFAP-positive) cortical astrocytes compared with control fetuses.
  
  
  CONCLUSIONS
  Vascular IUGR, as demonstrated in our asymmetric IUGR model, adversely affected brain growth, cell size, and cortical astrocytes maturation. In view of the neurotrophic and neuroprotective functions of astrocytes, a reduced number of mature astrocytes during this critical period of development may be implicated in the pathogenesis of the neurodevelopmental impairments observed in IUGR.
authors.affiliation: Pediatric Neurology and Child Development Unit, Dana Children's Hospital, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel. bassan@post.tau.ac.il
authors.forename: Haim
authors.initials: H
authors.lastname: Bassan
authors.forename: Debora
authors.initials: D
authors.lastname: Kidron
authors.forename: Merav
authors.initials: M
authors.lastname: Bassan
authors.forename: Michael
authors.initials: M
authors.lastname: Rotstein
authors.forename: Naam
authors.initials: N
authors.lastname: Kariv
authors.forename: Eliezer
authors.initials: E
authors.lastname: Giladi
authors.forename: Ariane
authors.initials: A
authors.lastname: Davidson
authors.forename: Illana
authors.initials: I
authors.lastname: Gozes
authors.forename: Shaul
authors.initials: S
authors.lastname: Harel
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000473:pathology* / Q000502:physiology; D001724:Birth Weight / Q000502:physiology; D001808:Blood Vessels / Q000473:pathology; D002452:Cell Count; D002540:Cerebral Cortex / Q000196:embryology / Q000473:pathology; D003251:Constriction, Pathologic; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology* / Q000503:physiopathology; D008026:Ligation; D021041:Placental Circulation / Q000502:physiology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000473:pathology* / Q000503:physiopathology; D011817:Rabbits