title: Characterization of the expression of macrophage inflammatory protein-1α (MIP-1α) and C-C chemokine receptor 5 (CCR5) after kainic acid-induced status epilepticus (SE) in juvenile rats.
abstract: OBJECTIVE
  To identify the potential role of macrophage inflammatory protein-1α (MIP-1α) 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-1α, 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-1α and CCR5 protein were quantified by ELISA and Western blot respectively following mRNA by real-time PCR. We also mapped MIP-1α 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-1α protein in hippocampus was transiently increased after KA treatment, and peaked from 16 to 72 h. Double-labelling immunofluorescence revealed that MIP-1α 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-1α and CCR5 expression were closely consistent with microglial accumulation in corresponding hippocampal subfields undergoing degenerative changes.
  
  
  CONCLUSIONS
  Our data indicated that MIP-1α 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.
authors.affiliation: Division of Neurology, Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, China.
authors.forename: X B
authors.initials: XB
authors.lastname: Zhu
authors.forename: Y B
authors.initials: YB
authors.lastname: Wang
authors.forename: O
authors.initials: O
authors.lastname: Chen
authors.forename: D Q
authors.initials: DQ
authors.lastname: Zhang
authors.forename: Z H
authors.initials: ZH
authors.lastname: Zhang
authors.forename: A H
authors.initials: AH
authors.lastname: Cao
authors.forename: S Y
authors.initials: SY
authors.lastname: Huang
authors.forename: R P
authors.initials: RP
authors.lastname: Sun
mesh_terms: D000818:Animals; D054405:Chemokine CCL3 / Q000235:genetics / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007608:Kainic Acid / Q000633:toxicity; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D019713:Receptors, CCR5 / Q000235:genetics / Q000378:metabolism*; D013226:Status Epilepticus / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology
chemical_list: D054405:Chemokine CCL3; D012333:RNA, Messenger; D019713:Receptors, CCR5; D007608:Kainic Acid