Region-specific plasticity in the epileptic rat brain: a hippocampal and extrahippocampal analysis.
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.
Jung
Keun-Hwa
KH
Department of Neurology, Stroke & Neural Stem Cell Laboratory in Clinical Research Institute, Stem Cell Research Center, Seoul National University, Seoul, South Korea.
Chu
Kon
K
Lee
Soon-Tae
ST
Kim
Jin-Hee
JH
Kang
Kyung-Muk
KM
Song
Eun-Cheol
EC
Kim
Se-Jeong
SJ
Park
Hee-Kwon
HK
Kim
Manho
M
Lee
Sang Kun
SK
Roh
Jae-Kyu
JK
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
D054377:Chemokine CXCL12; D010862:Pilocarpine; D018021:Lithium Chloride