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Immunohistochemical staining for glial fibrillary acidic protein (GFAP) after deafferentation or ischemic infarction in rat visual system: Features of reactive and damaged astrocytes
Author(s) -
SchmidtKastner R.,
Wietasch K.,
Weigel H.,
Eysel U.T.
Publication year - 1993
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(93)90076-p
Subject(s) - glial fibrillary acidic protein , pathology , superior colliculus , astrocyte , immunohistochemistry , gfap stain , lesion , biology , astrogliosis , ischemia , visual cortex , glial scar , anatomy , neuroscience , central nervous system , medicine
Immunohistochemical staining for glial fibrillary acidic protein (GFAP) is standard for visualization of reactive astrocytes in tissue sections, whereas various forms of astrocytic damage remain to be described in detail. In this study we tested differences in GFAP labeling in reactive astrocytes and in glial cells damaged by ischemia and edema. Studies were performed in the anatomically well defined visual system of rat. Basic staining patterns for GFAP were established in subcortical visual nuclei and visual cortex. In the first model, deafferentation of visual centers was performed by unilateral optic nerve lesion, and characteristic changes of GFAP labeling in reactive astrocytes were studied at 0.5,1,1.5,2,4,8 and 21 days after lesion. Initial changes were seen in the deafferented superior colliculus at 1 day after deafferentation with a diffuse increase and stellate types of reactive cells formed at 2–8 days. In the second model, small ischemie infarcts were produced in the visual cortex of rats using the method of photochemically‐induced thrombosis. GFAP labeling with a polyclonal antiserum was massively enhanced in the infarct at 4 hr. Characteristic morphological changes in damaged astrocytes were seen which were also identified in experiments with simulated global ischemia. In the surround of the infarct, swelling of astrocytes also caused increased labeling. At 3–4 days infarction typical reactive astrocytes surrounded the lesioned area. In conclusion, these immunohistochemical studies on GFAP in rat visual system allow for the following classifications, (a) Normal astrocytes vary in labeling at different anatomical localizations, (b) Reactive astrocytes show enhanced labeling and larger cell‐size within an interval of 1–2 days after lesion (c) Astrocytes damaged by ischemia reveal increased labeling of disintegrating cellular elements within hours after a lesion (d) Swollen astrocytes undergo enhanced labeling in areas with vasogenic edema.