CORTICOTROPIN-releasing hormone (CRH) antagonism has neuroprotective e
ffects in models of ischemia. We examined CRH mRNA by in situ hybridiz
ation in a well-established rat model of focal cerebral ischemia cause
d by permanent middle cerebral artery occlusion (MCAo). In ischemic co
rtex CRH mRNA levels were elevated 2.6-fold 60 min after MCAo, compare
d with sham operated animals. CRH mRNA was also induced in the amygdal
a, 60 min following ischemia, in a pattern which was qualitatively dif
ferent from that of sham operated animals. This rapid and profound inc
rease in CRH mRNA levels during focal cerebral ischemia is likely to b
e associated with neurotoxicity, as CRH antagonism has been reported t
o cause a significant reduction in neuronal loss during ischemia.