In the present studies, changes of the glial fibrillary acidic protein (GFAP) expression in the astrocytes of the rat hippocampal formation were examined in response to the bilateral carotid artery occlusion for 10 minutes along with a decrease of mean arterial blood pressure (MABP) to 50 mmHg. Their relations to neuronal viability were also studied by H&E staining. In early postischemic period, mild increase of the GFAP expression was observed and this was not only confined to the mild-necrotic (CA3 and dentate gyrus) regions but also in the non-necrotic regions (CA1 and subiculum) at postischemic 8 h. This suggest that astrocytosis during early postischemic period may be resulted from nonspecific reaction associated with changes in brain environment. In contrast, in late phase of the postischemia, a marked increase of the GFAP expression was observed at day 4. Moreover, cell bodies were significantly larger and many prominent and numerous processes were observed, suggesting that this may also contribute to the significant increase in the GFAP expression. Importantly, these cellular changes were only confined to the regions of massive necrosis such as subiculum and inner granular cell layer of dentate gyrus and were not observed in the non-necrotic regions (except CA1). In contrast, the GFAP expression in astrocytes were returned to control levels in mildly damaged CA3 region by 4 days. Thus reactive astrocytosis with upregulation of the GFAP in the late postischemic period with structural transformation in the regions of massive necrosis may contribute to the damages in the neighboring neurons.