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KMID : 0350519960490020661
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Journal of Catholic Medical College
1996 Volume.49 No. 2 p.661 ~ p.672
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GF AP-and Vimentin-Immunoreact6ivity of the Hippocampal Astrocytes in the Rat with 4-Pentenoic Acid-Induced Reye's Syndrome
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Abstract
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It is well known that 4-pentenoic acid(4-PA) is a neurotoxin to produce essential features of Rey's syndrome in rats, but little has been studied about the effects of this reagent on the changes of glial fibrillary acidic protein (GFAP) and
vimentin
(VIM) immunoreactivity of astrocytes in the experimented Reye's syndrome.
This study was designed to evaluate differences in the GFAP and VIM immunoreactivity, which are generally accepted as astrocyte-specific markers to brain injury and to brain injury and to find the different susceptibility depending on the
hippocampal
subfields (CA1, CA3, dentate gyrus, dentate hilus) in the early stage of experimented Reye's syndrome in the rat by light microscopic immunochemistry using anti-GFAP and VIM antiserum.
Reve's syndrome was induced by intraperitoneal injection every 4 hours with 50 mg/kg body weight of 4-PA for 10 doses, followed by a single dose of 200 mg/kg, and animals of each group were sacrificed at intervals of 12, 24, 48 and 72 hours after
the
final injection respectively. Control group was treated with normal saline. Tissue blocks were taken from hippocampus, whose paraffin sections were immunostained with the indirect immunoperoxidase method using anti-rabbit GFAP polyclonal antibody
and
anti-mouse VIM monoclonal antibody. The area percent of GFAP-positive astrocytes was calculated using the jmage analysing system (Vidas 2.0, Kontron, Germany) in the immunostained sections.
@ES The results were as follows:
@EN During the experimental period 12 to 72 hours after the 4-PA administration, the GFAP immunoreactivity and the area percent of GFAP-positive astrocytes were increased throughout the hippocampal subfields, especially CA3 and dentate hilus, as
compared with those of normal control. On the other hand, there was no VIM-positive astrocyte found until 48 hours, but a few VIM-positive astrocytes were observed in the CA3 and dentate hilus 72 hours after the 4-PA administration.
It is suggested that the difference of GFAP and VIM expression in acute stage of 4-PA induced-Reye's syndrome in not induced by an overt neuronal necrosis, but may reflect a compensatory reaction by a metabolic injury to the astrocyte.
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