期刊
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
卷 38, 期 6, 页码 602-616出版社
WILEY
DOI: 10.1111/j.1365-2990.2012.01251.x
关键词
chemokine; chemokine receptor; hippocampus; kainic acid; microglia; seizure
资金
- Natural Science Foundations of Shandong Province [Y2007C040]
X. B. Zhu, Y. B. Wang, O. Chen, D. Q. Zhang, Z. H. Zhang, A. H. Cao, S. Y. Huang and R. P. Sun (2012) Neuropathology and Applied Neurobiology38, 602616 Characterization of the expression of macrophage inflammatory protein-1a (MIP-1a) and C-C chemokine receptor 5 (CCR5) after kainic acid-induced status epilepticus (SE) in juvenile rats Aims: To identify the potential role of macrophage inflammatory protein-1a (MIP-1a) with its C-C chemokine receptor 5 (CCR5) in epileptogenic brain injury, we examined their expression in juvenile rat hippocampus and explored the potential link between MIP-1a, CCR5 and neuropathological alterations after status epilepticus (SE) induced by intracerebroventricular (i.c.v.) kainic acid (KA) injection. Methods: Based on the determination of the development of spontaneous seizures initiated by SE in developing rat brain, we firstly examined hippocampal neurone damage through Nissl and Fluoro-Jade B staining, and evaluated microglial reaction during the early phase following KA-induced SE in 21-day-old rats. MIP-1a and CCR5 protein were quantified by ELISA and Western blot respectively following mRNA by real-time PCR. We also mapped MIP-1a and CCR5 expression in the hippocampus by immunohistochemistry and identified their cellular sources using double-labelling immunofluorescence. Results: In juvenile rats, KA caused characteristic neurone damage in the hippocampal subfields, with accompanying microglial accumulation. In parallel with mRNA expression, MIP-1a protein in hippocampus was transiently increased after KA treatment, and peaked from 16 to 72 h. Double-labelling immunofluorescence revealed that MIP-1a was localized to microglia. Up-regulated CCR5 remained prominent at 24 and 72 h and was mainly localized to activated microglia. Further immunohistochemistry revealed that MIP-1a and CCR5 expression were closely consistent with microglial accumulation in corresponding hippocampal subfields undergoing degenerative changes. Conclusions: Our data indicated that MIP-1a as a regulator, linking with the CCR5 receptor, may be involved within the early stages of the epileptogenic process following SE by i.c.v. KA injection.
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