期刊
BRAIN RESEARCH
卷 1342, 期 -, 页码 138-149出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2010.04.046
关键词
Transient cerebral ischemia; Hippocampus; Neuronal degeneration; Microglial activation
资金
- Ministry of Education, Science and Technology [2009K001290, 2009-0094073]
- Republic of Korea
- National Research Foundation of Korea [2009-0094073] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Delayed neuronal death following transient cerebral ischemia is mixed with apoptosis and necrosis, and the activation of microglia are activated after the ischemic insult. In the present study, we examined the long-term changes in neuronal degeneration and microglial activation in the gerbil hippocampal CA1 region after 5 min of transient cerebral ischemia using specific markers for neuronal damage and microliosis. Transient ischemia-induced neuronal death was shown in CA1 pyramidal cells 4 days after ischemia/reperfusion (I/R). However, neuronal degeneration of the pyramidal cells were observed up to 45 days in the CA1 region after I/R. Microglial activation was also observed in the CA1 region after I/R. Isolectin B4- (IB4) immunore active ((+)) microglia appeared in the CA1 region 4 days after I/R. On the other hand, ionized calcium-binding adapter molecule 1 (Iba-1)(+) microglia was markedly increased after I/R, and peaked at 15 days after I/R. Thereafter, Iba-1 immunoreactivity was decreased with time-dependant manner in the ischemic CA1 region. These results indicate that neuronal degeneration of CA1 pyramidal cells may last about 45 days in the CA1 region after ischemic damage, and microgfial activation may be diverse according to their function, such as phagocytosis, after I/R. (C) 2010 Elsevier B.V. All rights reserved.
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