Document Detail


Prenatal ischemia and white matter damage in rats.
MedLine Citation:
PMID:  16254494     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ischemia/reperfusion injury to the developing brain is a major cause of neurologic abnormalities in preterm infants. To investigate the underlying mechanisms, we modified a previously described rat model of unilateral uterine-artery ligation on the 17th embryonic day (E17). Growth retardation was taken as an index of in utero ischemia, and pups born with a birth weight more than 2 standard deviations below that of controls were compared with the same-litter, normal-growth control pups born from the nonligated horn. Prenatal ischemia probably associated with hypoxia and followed by reperfusion at birth induced white matter damage at a developmental stage corresponding to extreme prematurity in humans. On P0 (day of birth), growth-retarded pups exhibited lesions in the cingular white matter and internal capsule with increased counts of activated microglial cells for 2 weeks compared with controls. Astrogliosis was detected in the injured white matter. On P3, increased apoptotic cell death was seen in O4-positive preoligodendrocytes, which were abnormally scarce on P7. Defective myelination, as assessed by myelin-binding-protein labeling, was detected until adulthood. The diffuse white matter damage in growth-retarded rats replicated the main features of white matter damage in human preterm infants.
Authors:
Paul Olivier; Olivier Baud; Philippe Evrard; Pierre Gressens; Catherine Verney
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuropathology and experimental neurology     Volume:  64     ISSN:  0022-3069     ISO Abbreviation:  J. Neuropathol. Exp. Neurol.     Publication Date:  2005 Nov 
Date Detail:
Created Date:  2005-10-28     Completed Date:  2005-12-15     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985192R     Medline TA:  J Neuropathol Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  998-1006     Citation Subset:  IM    
Affiliation:
INSERM U676-Université Paris7, Robert Debré Pediatric Hospital, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Antigens, CD11b / metabolism
Brain Diseases / metabolism,  pathology*
Caspase 3
Caspases / metabolism
Cell Count / methods
Cell Death
Disease Models, Animal
Embryo, Mammalian
Female
Gene Expression Regulation, Developmental / physiology
Glial Fibrillary Acidic Protein / metabolism
Glucose Transporter Type 2 / metabolism
Hypoxia-Ischemia, Brain / metabolism,  pathology*
Immunohistochemistry / methods
In Situ Nick-End Labeling / methods
Male
Myelin Basic Proteins / metabolism
Neovascularization, Pathologic / metabolism,  pathology
O Antigens / metabolism
Plant Lectins / metabolism
Pregnancy
Rats
Rats, Sprague-Dawley
Statistics, Nonparametric
Chemical
Reg. No./Substance:
0/Antigens, CD11b; 0/Glial Fibrillary Acidic Protein; 0/Glucose Transporter Type 2; 0/Myelin Basic Proteins; 0/O Antigens; 0/Plant Lectins; 0/tomato lectin; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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