The time-dependent effect of lipopolysaccharide on kainic acid-induced neuronal death in hippocampal CA3 region: possible involvement of cytokines via glucocorticoid

Abstract It has been reported that glucocorticoid (Gc) can induce neuronal cell toxicity in the hippocampus. In addition, we examined that serum Gc increased by restraint stress aggravated kainic acid (KA)-induced neuronal death in hippocampal CA3 region. However, the effect of other stressful stimu...

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Bibliographic Details
Published in:Neuroscience 2010-02, Vol.165 (4), p.1333-1344
Main Authors: Kwon, M.-S, Seo, Y.-J, Choi, S.-M, Won, M.-H, Lee, J.-K, Park, S.-H, Jung, J.-S, Sim, Y.-B, Suh, H.-W
Format: Article
Language:English
Subjects:
Animals
Astrocytes - drug effects
Astrocytes - physiology
Biological and medical sciences
CA3 Region, Hippocampal - drug effects
CA3 Region, Hippocampal - physiopathology
Cell Death - drug effects
Cell Death - physiology
Corticosterone - blood
Corticosterone - metabolism
cytokines
Cytokines - metabolism
Excitatory Amino Acid Agonists - toxicity
Fundamental and applied biological sciences. Psychology
glucocorticoid
hippocampus
Interleukin-1beta - metabolism
kainic acid
Kainic Acid - toxicity
Lipopolysaccharides - toxicity
LPS
Male
Mice
Mice, Inbred ICR
Microglia - drug effects
Microglia - physiology
Mifepristone - pharmacology
Neuroimmunomodulation - drug effects
Neuroimmunomodulation - physiology
Neurology
neuronal death
Neurons - drug effects
Neurons - physiology
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - metabolism
RNA, Messenger - metabolism
Time Factors
Vertebrates: nervous system and sense organs
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Summary:Abstract It has been reported that glucocorticoid (Gc) can induce neuronal cell toxicity in the hippocampus. In addition, we examined that serum Gc increased by restraint stress aggravated kainic acid (KA)-induced neuronal death in hippocampal CA3 region. However, the effect of other stressful stimulus like lipopolysaccharide (LPS) increasing serum Gc on KA-induced neuronal death was not elucidated until now. Thus, we examined the time course effect of LPS on KA-induced neuronal death in the hippocampal CA3 region of mice, especially to address the role of Gc and inflammatory mediators. In the present study, we found that an aggravating effect of LPS on KA-induced neuronal death was correlated with an alteration of hippocampal IL-1β mRNA level at all time points, and the serum Gc and hippocampal IL-1β mRNA level was peak at 90 min after LPS treatment (LPS 90 min) when the aggravating effect of LPS on KA-induced neuronal death was maximum. In addition, RU38486 (glucocorticoid receptor antagonist) decreased the hippocampal IL-1β mRNA level and abolished the aggravating effect of LPS on KA-induced neuronal death at LPS 90 min and 24 h. In the immunohistochemical study, we found activated and ramified microglia (OX-42) and astrocyte (GFAP) at 24 h after LPS treatment (LPS 24 h) in the hippocampus. These results suggest that Gc itself, cytokines triggered by Gc, or both appears to be involved in the LPS effect depending on LPS pretreatment time.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2009.11.060