title: Damage to neurons and oligodendrocytes in the hippocampal CA1 sector after transient focal ischemia in rats.
abstract: Focal brain lesions such as transient focal cerebral ischemia can lead to neuronal damage in remote areas, including the ipsilateral substantia nigra and hippocampus, as well as in the ischemic core. In this study, we investigated acute changes in the ipsilateral hippocampus from 1 up to 7 days after 90 min of transient focal cerebral ischemia in rats, using anti-NeuN (neuronal nuclei), anti-Cu/Zn-superoxide dismutase (Cu/Zn-SOD), anti-Mn-SOD, anti-neuronal nitric oxide synthase (nNOS), anti-inducible NOS (iNOS), anti-glial fibrillary acidic protein (GFAP), anti-ionized calcium-binding adaptor molecule 1(Iba 1) and anti-2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) antibodies. In our western blot and histochemical analyses, present results show that transient focal cerebral ischemia in rats can cause a severe and acute damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector. The present findings also demonstrate that the expression of iNOS produced by Iba 1-immunopositive microglia precedes the damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal cerebral ischemia. In contrast, our results suggest that increased reactive oxygen species (ROS) production during reperfusion cannot lead to damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector after transient focal cerebral ischemia, because of an insufficient expression of Cu/Zn-SOD and Mn-SOD. Our double-labeled immunohistochemical study demonstrates that the overexpression of iNOS produced by Iba 1-immunopositive microglia may play a pivotal role in the damage of neurons and oligodendrocytes in the ipsilateral hippocampal CA1 sector at an acute stage after transient focal cerebral ischemia.
authors.affiliation: Department of Neurobiology and Therapeutics, Institute of Health Biosciences, The University of Tokushima Graduate School, Sho-machi, Tokushima, Japan.
authors.forename: Hiroto
authors.initials: H
authors.lastname: Uchida
authors.forename: Yuki
authors.initials: Y
authors.lastname: Fujita
authors.forename: Misato
authors.initials: M
authors.lastname: Matsueda
authors.forename: Masahiro
authors.initials: M
authors.lastname: Umeda
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Matsuda
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kato
authors.forename: Jiro
authors.initials: J
authors.lastname: Kasahara
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Araki
mesh_terms: D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases / Q000378:metabolism; D000818:Animals; D056547:CA1 Region, Hippocampal / Q000201:enzymology / Q000473:pathology*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000473:pathology*; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D008840:Microfilament Proteins; D009474:Neurons / Q000473:pathology*; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009836:Oligodendroglia / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: C100745:Aif1 protein, rat; D002135:Calcium-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D007527:Isoenzymes; D008840:Microfilament Proteins; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase; D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases