Focal cerebral ischemia induces CRH mRNA in rat cerebral cortex and amygdala.
Corticotropin-releasing hormone (CRH) antagonism has neuroprotective effects in models of ischemia. We examined CRH mRNA by in situ hybridization in a well-established rat model of focal cerebral ischemia caused by permanent middle cerebral artery occlusion (MCAo). In ischemic cortex CRH mRNA levels were elevated 2.6-fold 60 min after MCAo, compared with sham operated animals. CRH mRNA was also induced in the amygdala, 60 min following ischemia, in a pattern which was qualitatively different from that of sham operated animals. This rapid and profound increase in CRH mRNA levels during focal cerebral ischemia is likely to be associated with neurotoxicity, as CRH antagonism has been reported to cause a significant reduction in neuronal loss during ischemia.
Clinical Neuroendocrinology Branch, NIMH, NIH, Bethesda, Maryland 20892-1284, USA.
M L
ML
Wong
S A
SA
Loddick
P B
PB
Bongiorno
P W
PW
Gold
N J
NJ
Rothwell
J
J
Licinio
D000679:Amygdala / Q000098:blood supply / Q000378:metabolism*; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000378:metabolism; D002539:Cerebral Arterial Diseases / Q000378:metabolism; D002540:Cerebral Cortex / Q000098:blood supply / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000235:genetics*; D015870:Gene Expression; D002546:Ischemic Attack, Transient; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley
D012333:RNA, Messenger; D003346:Corticotropin-Releasing Hormone