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The alterations of oligodendrocyte, myelin in corpus callosum, and cognitive dysfunction following chronic cerebral ischemia in rats.

Authors: Chida, Y  Kokubo, Y  Sato, S  Kuge, A  Takemura, S  Kondo, R  Kayama, T 
Citation: Chida Y, etal., Brain Res. 2011 Sep 26;1414:22-31. Epub 2011 Jul 20.
Pubmed: (View Article at PubMed) PMID:21864831
DOI: Full-text: DOI:10.1016/j.brainres.2011.07.026

Although the white matter lesions, so called leuko-araiosis, often seen in elderly people have been gaining attention due to their association with cognitive dysfunction (CD) and high risk of incident stroke, the pathological significance of these lesions still remains controversial. Therefore, in the present study, we investigated the alterations in oligodendrocytes (OLG), including oligodendrocytes progenitor cells (OPCs), myelin, and CD following chronic cerebral ischemia in rats. SD rats were subjected to bilateral common carotid artery occlusion. Immunohistochemical staining was performed at 2, 4, 6, 8, and 12weeks after the induction of ischemia with anti-NG2 (OPCs), anti-GST-pi (OLG), and anti-MBP antibodies in paramedian corpus callosum (CC). CD was assessed by the Morris water maze test. There was a significant decrease in the number of GST-pi positive cells at 2weeks after the start of ischemia compared with that seen in the sham group. There was a significant increase of the number of NG2 positive cells at 4weeks in the ischemia group compared with the sham group. In the ischemic group, the amount of MBP was observed to have decreased significantly at each time point compared with the sham group. CD was observed in the ischemic group than that in the sham group at all time points. Our results indicate that remyelination is strongly correlated with the recovery of cognitive dysfunction following chronic cerebral ischemia.

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CRRD Object Information
CRRD ID: 5686850
Created: 2012-01-27
Species: All species
Last Modified: 2012-01-27
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.