Recently, the ectopic expression of corticotropin-releasing factor (CRF) has been suggested as being associated with processes linked to neuronal injury and/or degeneration in response to a brain insult. However, there is little experimental data linking CRF directly to neuronal death induced by ischemia. Therefore, in the present study, we investigated the temporal and spatial alteration of CRF and its binding protein expressions in the hippocampus after transient ischemia. As a result, we found the selective increase of CRF immunoreactivity in the CA1 pyramidal cells and their processes at only 4 days post-ischemic insult. In contrast, CRF binding protein immunoreactivity was rarely detected in the CA1 region. These results suggest that transient ischemia may provoke selectively ectopic expression of CRF, but not of its binding protein, in vulnerable regions, and this enhancement of CRF may play important roles in the neurodegenerative process.