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Neuronal loss and gliosis in the rat striatum subjected to 15 and 30 minutes of middle cerebral artery occlusion

Authors
Park, Joon HaCho, Jeong HwiAhn, Ji HyeonChoi, Soo YoungLee, Tae-KyeongLee, Jae-ChulShin, Bich NaHong, SeongkweonJeon, Yong HwanKim, Young-MyeongHwang, In KooLee, Young JooWon, Moo-HoKang, Il Jun
Issue Date
Jun-2018
Publisher
Kluwer Academic/Plenum Publishers
Keywords
Middle cerebral artery occlusion; Caudate putamen; Selective neuronal death; Fluoro Jade B; Astrocytes; Microglia
Citation
Metabolic Brain Disease, v.33, no.3, pp 775 - 784
Pages
10
Journal Title
Metabolic Brain Disease
Volume
33
Number
3
Start Page
775
End Page
784
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5930
DOI
10.1007/s11011-018-0192-8
ISSN
0885-7490
1573-7365
Abstract
Selective neuronal death or loss in certain brain regions has been well characterized in animal models of transient global cerebral ischemia. However, selective neuronal death in transient focal cerebral ischemia needs more investigation. Therefore, in this study, we studied selective neuronal death in the striatum (caudate putamen) of rats subjected to 15 or 30 min middle cerebral artery occlusion (MCAO). Neuronal death occurred in the dorsolateral field, not in the medial field in 30 min, not 15 min, MCAO-operated rats 5 days after MCAO using neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In this group, immunoreactivity of glial fibrillary acidic protein in astrocytes was hardly shown in the dorsolateral field, although the immunoreactivity increased in the medial field. In addition, immunoreactivity of ionized calcium binding adapter molecule 1 in microglia was dramatically increased in the dorsolateral, not in the medial, field only in 30 min MCAO-operated rats. Briefly, these results show that at least 30 min of MCAO can evoke selective neuronal death, astrocytic dysfunction and microglial activation in the dorsolateral field of the rat striatum and suggest that a rat model of 30 min MCAO can be used to investigate mechanisms of neuronal death and gliosis following brief transient focal cerebral ischemic events for acute transient ischemic attack.
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