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Differential activation of microglia and astrocytes in aniso‐ and isomorphic gliotic tissue
Author(s) -
FernaudEspinosa Isabel,
NietoSampedro M.,
Bovolenta P.
Publication year - 1993
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440080408
Subject(s) - gliosis , lesion , microglia , neuroglia , parenchyma , neuroscience , astrocyte , biology , hippocampus , pathology , glial scar , central nervous system , medicine , inflammation , immunology
Reactive astrocytes and microglial cells are both involved in the formation of gliotic tissue. Using immunohistochemical markers, we have compared the response of both these cell types after two different kinds of damage in the brain: traumatic injury (anisomorphic gliosis) and neurotoxic induced lesion (isomorphic gliosis), in two distinct regions of the brain, the cortex and the hippocampus. We show that the time course and the relative contribution of astrocytes and microglial cells differ greatly in the two kinds of lesions. While in anisomorphic gliosis there is little activation of endogenous microglial cells independently of the brain region damaged, these cells contribute in large measure and for prolonged periods of time to the formation of isomorphic gliotic tissue. Astrocytes are quickly activated at the border of anisomorphic lesions, and after 3 days they already occupy an extensive portion of the brain parenchyma. However, after 1 month, they are found restricted to a thin strip at the lesion boundary. In contrast, after an isomorphic lesion, astrocytes become reactive around the site of neuronal cell loss but not at the site of the lesion itself. Only after 2 weeks do they totally invade the damaged region, persisting for at least 1 month. Such differences are observed independently of the brain region damaged. These results suggest that the cellular, and therefore the molecular, composition of gliotic tissue depends on the type of insult the CNS has suffered. © 1993 Wiley‐Liss, Inc.