Abstract
Astrocytes play vital roles not only in the mechanical support of the central nervous system but also in the metabolism of neurotransmitters and in the transfer of nutritive substances to neuron. After ischemic brain injuries, it has been known that gliosis appears around degenerative regions and repairs these regions. Recently, accumulating evidence indicates that overexpression of S-100 protein, astrocyte-derived protein, is detrimental to neuronal cells in various pathological conditions. To confirm the astrocytic activation in cerebral ischemia, we examined immunohistochemical changes in S-100 protein and glial fibrillary acidic protein (GFAP) in the transient focal ischemia. Cerebral infarction determined by hematoxylin-eosin staining was slight on day 1 and further expanded on day 2 and 3. Thereafter, GFAP immunoreactivity was observed in boundary zone of the infarct area at 72 hours after the transient focal ischemia. On the other hand, S-100 protein immunoreactivities were markedly increased at 9 hours after the transient focal ischemia. After the infarct formation, the increase of S-100 immunoreactivity was observed in outside boundary of infarct area. These results suggest that astrocytic activation, which we would like to be called “pre-mitotic S-100 peak (PSP)”, precedes the neurodegeneration following the transient focal ischemia, and should be distinguished from so-called gliosis observed in the post-neurodegeneration and GFAP-dependent astrocytic proliferation.
