title: Myelination deficits in brain of rats following perinatal asphyxia.
abstract: Perinatal asphyxia remains a major cause of acute mortality and of permanent neurodevelopmental disability in infants and children. However, the pathophysiologic features of hypoxic-ischemic encephalopathy are still incompletely understood. Animal studies have been focussing on grey matter pathology but information on white matter lesions is limited. The aim of the study was to investigate white matter lesions after three months following graded perinatal asphyxia in the rat using a well-documented, reproducible, clinically relevant and simple animal model of perinatal asphyxia. Brains of rat pups (n=10 per group) exposed to asphyctic periods of 10 and 20 minutes were examined histologically and compared to normoxic brain using Kluever-Barrera myelin staining, immunohistochemically with antibodies against myelin basic protein, 2',3'-cyclic-nucleotide'-phosphodiesterase as markers for myelination, antibodies against neurofilaments for the evaluation of axonal density and antibodies against glial fibrillary acidic protein as a marker for astrocytic gliosis. Morphometry three months after perinatal asphyxia showed significant reduction of corpus callosum in asphyctic brains. Patchy myelination deficits were found in hippocampal fimbriae and cerebellum, lobulus L 8, accompanied by reduced axonal density. Hypothalamus and striatum did not show any myelination deficit. Up to now only short term effects of perinatal asphyxia on myelination have been reported and this communication reveals long-term myelination deficit in three brain regions after three months following perinatal asphyxia. As myelination deficit was regularly accompanied by reduction of neurofilament immunoreactivity, we suggest that white matter lesions are paralleling grey matter damage, a subject still controversial in pathophysiology of brain damage in perinatal asphyxia.
authors.affiliation: University of Vienna, Institute of Animal Breeding, Austria.
authors.forename: C
authors.initials: C
authors.lastname: Kohlhauser
authors.forename: W
authors.initials: W
authors.lastname: Mosgöller
authors.forename: H
authors.initials: H
authors.lastname: Höger
authors.forename: B
authors.initials: B
authors.lastname: Lubec
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001237:Asphyxia / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism; D001369:Axons / Q000473:pathology; D002452:Cell Count; D003711:Demyelinating Diseases / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D002534:Hypoxia, Brain / Q000378:metabolism / Q000473:pathology*; D007124:Immunoenzyme Techniques; D009186:Myelin Sheath / Q000378:metabolism / Q000473:pathology*; D016900:Neurofilament Proteins / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D005904:Glial Fibrillary Acidic Protein; D016900:Neurofilament Proteins