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Neuronal damage and gliosis in the somatosensory cortex induced by various durations of transient cerebral ischemia in gerbils

Authors
Lee, Jae-ChulAhn, Ji HyeonLee, Dae HwanYan, Bing ChunPark, Joon HaKim, In HyeCho, Geum-SilKim, Young-MyeongLee, BongheePark, Chan WooCho, Jun HwiLee, Hui YoungWon, Moo-Ho
Issue Date
13-May-2013
Publisher
ELSEVIER SCIENCE BV
Keywords
Ischemia-reperfusion; Ischemic duration; Cerebral cortex; Delayed neuronal death; Astrocytes; Microglia
Citation
BRAIN RESEARCH, v.1510, pp.78 - 88
Journal Title
BRAIN RESEARCH
Volume
1510
Start Page
78
End Page
88
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/14542
DOI
10.1016/j.brainres.2013.03.008
ISSN
0006-8993
Abstract
Although many studies regarding ischemic brain damage in the gerbil have been reported, studies on neuronal damage according to various durations of ischemia-reperfusion (I-R) have been limited. In this study, we examined neuronal damage/death and glial changes in the somatosensory cortex 4 days after 5, 10 and 15 min of transient cerebral ischemia using the gerbil. To examine neuronal damage, we used Fluoro-jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining as well as cresyl violet (CV) staining and neuronal nuclei (NeuN, neuronal marker) immunohistochemistry. In the somatosensory cortex, some CV and NeuN positive ((+)) neurons were slightly decreased only in layers III and VI in the 5 min ischemia-group, and the number of CV+ and NeuN(+) neurons were decreased with longer ischemic time. The F-J B histofluorescence staining showed a clear neuronal damage in layers III and VI, and the number of F-J B+ neurons was increased with time of ischemia-reperfusion: in the 15 min ischemia-group, the number of F-J B+ neurons was much higher in layer III than in layer VI. In addition, we immunohistochemically examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti-ionized calcium-binding adapter molecule 1 (Iba-1) antibody, respectively. In the 5 min ischemia-group, GFAP(+) astrocytes and Iba-1(+) microglia were distinctively increased in number, and their immunoreactivity was stronger than that in the sham-group. In the 10 and 15 min ischemia-groups, numbers of GFAP(+) and Iba-1(+) glial cells were much more increased with time of ischemia-reperfusion; in the 15 min ischemia-group, their distribution patterns of GFAP(+) and Iba-1(+) glial cells were similar to those in the 10 min ischemia-group. Our fining indicates that neuronal death/damage and gliosis of astrocytes and microglia were apparently increased with longer time of ischemia-reperfusion. (C) 2013 Elsevier B.V. All rights reserved.
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