Recently, we suggested that the ectopic expression of
corticotropin-releasing factor (CRF) is associated with processes linked to neuronal injury and/or degeneration in response to an ischemic insult. However, little experimental data currently links the
CRF receptor directly to neuronal death induced by
ischemia. Therefore, in the present study, we investigated the temporal and spatial changes in
CRF receptor immunoreactivity in the hippocampus and the neocortex after transient
ischemia.
CRF receptor immunoreactivity in the hippocampus was reduced up to 24h after
ischemia insult, as compared to the
sham. Interestingly,
CRF receptor immunoreactivity disappeared in the CA1 region of the hippocampus at 4 days in the post-ischemic group. The other regions of hippocampus maintained their immunoreactivities at this time point. On the other hand, in the neocortex, 3h after transient
ischemia, the
CRF receptor immunoreactivity was elevated in regions vulnerable to
ischemia. At 12h post-
ischemia, its immunoreactivity had decreased versus the
sham operated animals. These results suggest that the selectively ectopic expression of CRF following
ischemia, which we reported previously, may regulate inflammatory responses. In addition, these findings also suggest that the mechanisms of neuronal death as mediated by
CRF receptor differ in the hippocampus and the neocortex.