title: Expression of NGFI-B mRNA in a rat focal cerebral ischemia-reperfusion model.
abstract: Cerebral ischemia is known to induce the expression of several immediate early genes (IEGs), including c-fos and c-jun, which subsequently regulate a number of late effector genes. In this study, we examined the expression of NGFI-B (or nur 77) mRNA in a rat focal cerebral ischemia-reperfusion model. NGFI-B is a member of the IEGs which encodes for a nuclear receptor and is rapidly induced by nerve growth factor (NGF). Northern blot analysis showed a rapid but transient enhancement of NGFI-B mRNA, a peak level for which was observed at 30 min of reperfusion following 60 min ischemic insult. At the peak level, quantitative analysis of the blot indicated a 12-fold and 4-fold increase of NGFI-B mRNA in the ischemic cortex and ipsilateral hippocampus, respectively, as compared to the sham-operated control. No apparent changes in mRNA levels were observed within contralateral sites of the cortex. Results from in situ hybridization showed that severe ischemia (60 min) resulted in a marked increase of NGFI-B mRNA throughout the entire ischemic cerebral cortex. The increase was particularly notable in the frontal, occipital, perirhinal and piriform cortical regions and in the dentate gyrus and CAI-3 regions of the ipsilateral hippocampus. A marked induction was also noted in the ipsilateral caudate putamen. Unlike the induction profile of NGFI-B mRNA, severe ischemia resulted in bilateral increases of its family gene, NGFI-A mRNA. The spatial induction profile is similar to that of NGFI-B mRNA in both hemispheres, except within the region of the contralateral dentate gyrus which showed low levels of NGFI-A mRNA. The expression pattern of NGF and BDNF mRNA, upstream genes of NGFI-B, were also examined. Interestingly the temporal and spatial expression patterns of BDNF mRNA were very similar to that of NGFI-A mRNA under the same conditions, whereas increased NGF and NGFI-B mRNA were observed only in the ipsilateral hemisphere. It is likely that multiple and/or overlapping pathways are activated subsequent to ischemic challenge which in turn are crucial for cel survival and/or functional recovery following focal cerebral ischemia.
authors.affiliation: Division of Neuroscience, Academia Sinica, Taipei, Taiwan, ROC. bmltn@ibms.sinica.edu.tw
authors.forename: T N
authors.initials: TN
authors.lastname: Lin
authors.forename: J J
authors.initials: JJ
authors.lastname: Chen
authors.forename: S J
authors.initials: SJ
authors.lastname: Wang
authors.forename: J T
authors.initials: JT
authors.lastname: Cheng
authors.forename: S I
authors.initials: SI
authors.lastname: Chi
authors.forename: A B
authors.initials: AB
authors.lastname: Shyu
authors.forename: G Y
authors.initials: GY
authors.lastname: Sun
authors.forename: C Y
authors.initials: CY
authors.lastname: Hsu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D017403:In Situ Hybridization; D008297:Male; D009414:Nerve Growth Factors / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats
chemical_list: D009414:Nerve Growth Factors; D012333:RNA, Messenger