title: The alterations of oligodendrocyte, myelin in corpus callosum, and cognitive dysfunction following chronic cerebral ischemia in rats.
abstract: 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-π (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-π 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.
authors.affiliation: Department of Neurosurgery, Yamagata University, Faculty of Medicine, 2-2-2 Iida-nishi, Yamagata 990-9585, Japan.
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Chida
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Kokubo
authors.forename: Shinya
authors.initials: S
authors.lastname: Sato
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kuge
authors.forename: Sunao
authors.initials: S
authors.lastname: Takemura
authors.forename: Rei
authors.initials: R
authors.lastname: Kondo
authors.forename: Takamasa
authors.initials: T
authors.lastname: Kayama
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000941:Antigens / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications*; D001973:Bromodeoxyuridine / Q000378:metabolism; D002452:Cell Count; D002908:Chronic Disease; D003072:Cognition Disorders / Q000209:etiology* / Q000473:pathology*; D003337:Corpus Callosum / Q000473:pathology*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D018782:Maze Learning / Q000502:physiology; D004676:Myelin Basic Protein / Q000378:metabolism; D009186:Myelin Sheath / Q000473:pathology*; D009836:Oligodendroglia / Q000473:pathology*; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000378:metabolism; D013997:Time Factors; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D001973:Bromodeoxyuridine; D004676:Myelin Basic Protein; D011509:Proteoglycans; D020796:Receptor, Platelet-Derived Growth Factor alpha; D000099216:Chondroitin Sulfate Proteoglycan 4