It is generally accepted that astrocytes are highly resistant to ischemic insults. But a specific loss of glial fibrillary acidic protein (GFAP) and immunolabeling in protoplasmic astrocytes occurred within minutes in the area with total depletion of regional blood flow, whereas "classic" gliosis was observed in areas with remaining cerebral blood flow (Lukaszevicz et al. 2002; Zhao et al. 2003). Severe disturbance of cell function, as suggested by decreased GFAP content and increased permeability of the blood-brain barrier to macromolecules, was rapidly followed by necrotic cell death.
Astrocytic alterations as demonstrated by cyto-plasmic swelling (ameboid glia) are demonstrable within 2-5 h (Müller 1930; Rand and Courville 1932; Blakemore 1971). Hypertrophic astrocytes with eccentric nuclei are first seen 6 days after ischemia
(Link and Schleussing 1955; Schröder 1983), in the cornu Ammonis (Figs. 14.8a, 9), cerebral cortex (Fig. 14.8c), the cerebral white matter (Fig. 14.10a, b), and cerebellar cortex (Fig. 14.10c, d). Moreover, in the cerebellar cortex an increase of glial fibers is demonstrable replacing lost Purkinje cells (Fig. 14.10b, c).
The astrocytic activation is extensively described by Archer and Walz (2000), who could demonstrate upregulation of GFAP as a first expression of reactivity associated with an increase of GFAP-re-active astrocytic mitosis. The astrocytic activation obviously is protective to neurons subjected to an ischemic insult (Louw et al. 1998). Moreover, a local gliotic response could be distinguished from a remote gliotic response. Schwab et al. (2000) could demonstrate that the number of astrocytes expressing connective tissue growth factors was significantly higher in border zones adjacent to the core, corresponding to the penumbra. These numbers were significantly increased in the first and third days and remained persistently elevated up to several months post infarction.
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