Abstract
It is not entirely clear whether the proliferative changes in astrocytes following cerebral ischemia are in response to neuronal injury or are secondary to the direct effects of ischemia on the astrocytes. Therefore, the following study examined the relationship between post‐ischemic astrocytosis with the extent of neuronal necrosis and the severity of the ischemia. Astrocyte reactivity was assessed by alterations in glial fibrillary acidic protein (GFAP), using immunohistochemistry and evaluation by optical density analysis. Cerebral ischemia was produced in rats by temporary occlusion of the carotid and vertebral arteris for 2,10 and 30 min. This results in damage to the CA1 neurons after a characteristic delay of several days, the duration of which is inversely proportional to the severity of the ischemia. CA3 neurons are resistant to the ischemia and do not suffer permanent injury. The results showed that GFAP immunoreactivity significantly increased in the CA1 region after all three ischemic intervals but the rise of GFAP in the CA3 area reached significance only after 30 min of ischemia. The peak and duration of the GFAP increases thus correlated with the extent and the maturation of the neuronal necrosis. This suggests that with mild injury (2 and 10 min ischemia), post‐ischemic astrocytosis is closely related to its neuronal environment rather than to the ischemic insult itself. Furthermore, the results showed an initial decrease in and delay of the subsequent GFAP rise. This initial decline in GFAP and the delay in its rise have both been identified in other models of brain injury and may be related in part to transient astrocyte swelling as well as to a finite interval required for sufficient increases in transcriptional activity to affect a noticeable rise in GFAP immunoreactivity.
