title: Region-specific plasticity in the epileptic rat brain: a hippocampal and extrahippocampal analysis.
abstract: OBJECTIVE
  Recent evidence suggests that aberrant neuro/gliogenesis and/or inflammation play critical roles in epileptogenesis. Although the plastic and inflammatory changes have been described in the postseizure hippocampus, little data is available concerning extrahippocampal regions, notably in the piriform and entorhinal cortices, amygdala, and parts of the thalamus. In this study, we examined histological changes in whole epileptic rat brain, with respect to cell death, cell genesis, and inflammation.
  
  
  RESULTS
  Experimental status epilepticus (SE) was induced using a lithium-pilocarpine injection. Neuronal death was evident in the amygdala, piriform, and entorhinal cortices, as well as the subfields of hippocampus. Microglial activation was observed in more extended limbic areas, such as, the hippocampus, entorhinal, perirhinal and piriform cortices, amygdala, thalamus, and hypothalamus, and a robust increase of cell genesis was noted in these damaged areas. The majority of newly generated cells in extrahippocampal areas proliferated in situ, and differentiated mainly into astrocytes or oligodendrocytes. In addition, stromal cell-derived factor-1alpha was found to be induced in close temporal and anatomical association with seizure-induced plasticity.
  
  
  CONCLUSIONS
  These findings indicate that neuronal death, inflammation, and cell genesis are substantially associated throughout the entire brain and that they may influence the epileptogenic process and clinical manifestations.
authors.affiliation: Department of Neurology, Stroke & Neural Stem Cell Laboratory in Clinical Research Institute, Stem Cell Research Center, Seoul National University, Seoul, South Korea.
authors.forename: Keun-Hwa
authors.initials: KH
authors.lastname: Jung
authors.forename: Kon
authors.initials: K
authors.lastname: Chu
authors.forename: Soon-Tae
authors.initials: ST
authors.lastname: Lee
authors.forename: Jin-Hee
authors.initials: JH
authors.lastname: Kim
authors.forename: Kyung-Muk
authors.initials: KM
authors.lastname: Kang
authors.forename: Eun-Cheol
authors.initials: EC
authors.lastname: Song
authors.forename: Se-Jeong
authors.initials: SJ
authors.lastname: Kim
authors.forename: Hee-Kwon
authors.initials: HK
authors.lastname: Park
authors.forename: Manho
authors.initials: M
authors.lastname: Kim
authors.forename: Sang Kun
authors.initials: SK
authors.lastname: Lee
authors.forename: Jae-Kyu
authors.initials: JK
authors.lastname: Roh
mesh_terms: D000679:Amygdala / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D054377:Chemokine CXCL12 / Q000032:analysis; D018728:Entorhinal Cortex / Q000473:pathology / Q000503:physiopathology*; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D018021:Lithium Chloride; D008297:Male; D017628:Microglia / Q000473:pathology / Q000502:physiology; D055495:Neurogenesis / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009836:Oligodendroglia / Q000473:pathology / Q000502:physiology; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D013788:Thalamus / Q000473:pathology / Q000503:physiopathology*; D015854:Up-Regulation / Q000502:physiology
chemical_list: D054377:Chemokine CXCL12; D010862:Pilocarpine; D018021:Lithium Chloride