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Nestin expression in hippocampal astrocytes after injury depends on the age of the hippocampus
Author(s) -
AbdelRahman Ali,
Rao Muddanna S.,
Shetty Ashok K.
Publication year - 2004
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.20047
Subject(s) - nestin , glial fibrillary acidic protein , biology , hippocampal formation , astrocyte , kainic acid , neuroscience , hippocampus , neuroglia , neurodegeneration , glial scar , astrogliosis , lesion , pathology , central nervous system , glutamate receptor , neural stem cell , medicine , immunohistochemistry , microbiology and biotechnology , immunology , stem cell , biochemistry , receptor , disease
Analysis of the expression of nestin in reactive astrocytes facilitates quantification of the extent of activation of astrocytes after injury in the mature CNS. We hypothesize that the capability of astrocytes for re‐expressing nestin in response to CNS injury diminishes as a function of age. We quantified astrocytes positive for S‐100β protein, glial fibrillary acidic protein (GFAP) and nestin in the hippocampus of young adult, middle‐aged, and aged Fischer 344 rats after an intracerebroventricular kainic acid (KA) administration. In all age groups, KA administration induced degeneration of CA3 pyramidal neurons, which led to a significant deafferentation in the CA1 region. The KA‐induced neurodegeneration and deafferentation resulted in an increased population of astrocytes positive for S‐100β and glial fibrillary acidic protein (GFAP) in all age groups. Interestingly, these increases were highly comparable across the three age groups. However, in areas of both neurodegeneration and deafferentation, the overall numerical density of nestin‐positive reactive astrocytes varied depending on the age at the time of injury with noticeably decreased numerical density in the injured middle‐aged and aged hippocampus. In contrast, nestin‐immunoreactive radial glia framework after lesion is not impaired with aging in the ependymal lining of the CA3 region. © 2004 Wiley‐Liss, Inc.