Delayed transhemispheric c-fos gene expression after focal cerebral ischemia-reperfusion in rats.
Using a unilateral, focal, cortical, ischemia-reperfusion rat model, c-fos mRNA and Fos immunoreactivity in the brain were investigated. The study was divided into a series of reperfusion intervals which were carried out for a period of up to 7 days. The c-fos mRNA peaked in the ischemic cortex (about 15-fold) after 30 minutes of ischemia followed by 1 hour of reperfusion and dropped to baseline level after 1 day of reperfusion. Increased expression switched to the bilateral retrosplenial and frontal cortex, as well as the left (nonischemic) parietal cortex, at 3- or 5-days of reperfusion (about three- to fourfold). Fos immunohistochemical staining correlated positively with the surge of c-fos mRNA. Nuclear run-off transcription assays further indicated that the increase in c-fos mRNA was regulated at the transcriptional level not only in the ischemic cortex (30 min of ischemia, followed by 1 h of reperfusion) but also in the contralateral counterpart (30 min of ischemia, followed by 3 d of reperfusion). A link between altered gene expression and diaschisis is suggested. The distant/delayed c-fos expression is probably caused by loss of inhibition from the ischemic cortex through a polysynaptic transneural pathway.
Liu
J S
JS
Department of Neurology, Kaohsiung Medical College, Taiwan ROC.
Chang
Y Y
YY
Chen
W H
WH
Chen
S S
SS
D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply / Q000378:metabolism*; D015870:Gene Expression; D016762:Genes, fos; D002546:Ischemic Attack, Transient / Q000235:genetics*; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion
D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger