FOCAL CEREBRAL-ISCHEMIA INDUCES CRH MESSENGER-RNA IN RAT CEREBRAL-CORTEX AND AMYGDALA

被引：45

作者：

WONG, ML ^{[1
]}

LODDICK, SA ^{[1
]}

BONGIORNO, PB ^{[1
]}

GOLD, PW ^{[1
]}

ROTHWELL, NJ ^{[1
]}

LICINIO, J ^{[1
]}

机构：

[1] UNIV MANCHESTER,SCH BIOL SCI,MANCHESTER M13 9PT,LANCS,ENGLAND

来源：

NEUROREPORT | 1995年 / 6卷 / 13期

基金：

英国惠康基金;

关键词：

CORTICOTROPIN-RELEASING HORMONE; CEREBRAL ISCHEMIA; CEREBRAL CORTEX; AMYGDALA; PARAVENTRICULAR HYPOTHALAMIC NUCLEUS; IN SITU HYBRIDIZATION; DENSITOMETRY;

D O I：

10.1097/00001756-199509000-00019

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：1785 / 1788

页数：4

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