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KMID : 0350519950480020485
Journal of Catholic Medical College
1995 Volume.48 No. 2 p.485 ~ p.501
Alterations of GFAP-Immunoreactive Astrocytes in the Brain of the Rat with Reye's Syndrome Induced by 4-Pentenoic Acid


Abstract
4-pentenoic acid (4-PA) has been known to be a useful neurotoxin to produce most of the essential features of Reye's syndrome in rats (Glasgow & Chase, 1975 ; Yoshida et al., 1979), but little has been studied about the effects of this reagent on
the
changes of the glial fibrillary acidic protein (GFAP) immunoreactivity of astrocytes in the central nervous system.
We designed this study in order to clarify the alterations of the GFAP-immunoreacitvity, area percent and ultrastructure of GFAP-positive astrocytes in the brain of the rat with experimental Reye's syndrome by light and electron microscopic
immunocytochemistry using anti-GFAP antiserum.
Reye's syndrome was induced by intraperitoneal injection every 4 hr with 50mg/kg body weight of 4-PA for 10 doses, followed by a single dose of 200mg/kg. Animals were sacrificed in 30 minutes after the final injection, and tissue blocks were
taken
from
the cerebrum and cerebellum. Paraffin sections were immunostained with the indirect immunoperoxidase method for light microscopy, and the area percent of GFAP-positive astrocytes was calculated using the image analysing system (Vidas 2.0 Kontron,
German) in the immunostained sections. For electron microscopy, pee-embedding immunocytochemical method was applied.
@ES The results were as follows :
@EN During the experimental period, all rate were observed clinical features similar to those of the Reye's syndrome, including convulsion, hyperammonemia, hypoglycemia and elevated SGOT. The GFAP immunoreactivity and the area percent of
GFAP-positive
astrocytes in 4-PA-treated animals were significantly increased in cerebral cingulum and cerebellar cortex and medulla, as compared with those of normal control. The increment was highly significant in cerebellum than in cerebrum. However, the
intensity
was observed to be siight in frontal cortex.
The intermediate filaments in the cytoplasm of astrocytes were selectively immunostained by the electron microscopic immunocytochemistry and these GFAP-immunoreactive intermediate filaments were markedly increased in both cerebral and cerebellar
astrocytes of the 4-PA-treated animals.
In conclusion, these observations elucidate that the increment of GFAP expression and intermediate filaments in the astrocytes of the early stage of Reye's syndrome induced by 4-PA, and suggest that the compensatory reactive astrocytosis is
consequently
involved in the encephalopathy.
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