Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

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• 作者：Taek Geun Ohk (1)
  Ki-Yeon Yoo (2)
  Seung Min Park (1)
  Bich Na Shin (3)
  In Hye Kim (3)
  Joon Ha Park (3)
  Hee Cheol Ahn (1)
  Young Joo Lee (4)
  Myong Jo Kim (5)
  Tae Young Kim (6)
  Moo-Ho Won (3) mhwon@kangwon.ac.kr
  Jun Hwi Cho (7) cjhmd@kangwon.ac.kr
• 关键词：Ischemia&#8211 ; reperfusion &#8211 ; Ischemic duration &#8211 ; Fluoro ; Jade B &#8211 ; Astrocytes &#8211 ; Microglia
• 刊名：Neurochemical Research
• 出版年：2012
• 出版时间：April 2012
• 年：2012
• 卷：37
• 期：4
• 页码：826-834
• 全文大小：807.0 KB
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• 作者单位：1. Department of Emergency Medicine, Hallym University Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, 431-070 South Korea2. Department of Oral Anatomy, College of Dentistry, Gangneung-Wonju National University, Gangneung, 210-702 South Korea3. Department of Neurobiology, and Institute of Medical Sciences, School of Medicine, Kangwon National University, Chuncheon, 200-701 South Korea4. Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University, Seoul, 140-743 South Korea5. Oriental Bio-herb Research Institute, Kangwon National University, Chuncheon, 200-701 South Korea6. Fermentation & Food Processing, Department of Korean Food Research for Globalization, NAAS, RDA, Suwon, 441-707 South Korea7. Department of Emergency Medicine, and Institute of Medical Sciences, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon, 200-701 South Korea
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Ischemic damage occurs well in vulnerable regions of the brain, including the hippocampus and striatum. In the present study, we examined neuronal damage/death and glial changes in the striatum 4 days after 5, 10, 15 and 20 min of transient cerebral ischemia using the gerbil. Spontaneous motor activity was increased with the duration time of ischemia–reperfusion (I-R). To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. F-J B positive cells were detected only in the 20 min ischemia-group, not in the other groups. In addition, we examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti- ionized calcium-binding adapter molecule 1 (Iba-1), respectively. In the 5 min ischemia-group, GFAP-immunoreactive astrocytes were distinctively increased in number, and the immunoreactivity was stronger than that in the sham-group. In the 10, 15 and 20 min ischemia-groups, GFAP-immunoreactivity was more increased with the duration of I-R. On the other hand, the immunoreactivity and the number of Iba-1-immunoreactive microglia were distinctively increased in the 5 and 10 min ischemia-groups. In the 15 min ischemia-group, cell bodies of microglia were largest, and the immunoreactivity was highest; however, in the 20 min ischemia-group, the immunoreactivity was low compared to the 15 min ischemia-group. The results of western blotting for GFAP and Iba-1 were similar to the immunohistochemical data. In brief, these findings showed that neuronal death could be detected only in the 20 min ischemia-group 4 days after I-R, and the change pattern of astrocytes and microglia were apparently different according to the duration time of I-R.