The effects of vascular intrauterine growth retardation on cortical astrocytes.
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.
Bassan
Haim
H
Pediatric Neurology and Child Development Unit, Dana Children's Hospital, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel. bassan@post.tau.ac.il
Kidron
Debora
D
Bassan
Merav
M
Rotstein
Michael
M
Kariv
Naam
N
Giladi
Eliezer
E
Davidson
Ariane
A
Gozes
Illana
I
Harel
Shaul
S
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