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    Glial activation links early-life seizures and long-term neurologic dysfunction: evidence using a small molecule inhibitor of proinflammatory cytokine upregulation

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    Authors
    Somera-Molina, Kathleen C.
    Robin, Beverley
    Somera, Cherie Ann
    Anderson, Christopher
    Stine, Christy D.
    Koh, Sookyoung
    Behanna, Heather A.
    Van Eldik, Linda J.
    Watterson, D. Martin
    Wainwright, Mark S.
    UMass Chan Affiliations
    Department of Pediatrics
    Document Type
    Journal Article
    Publication Date
    2007-09-01
    Keywords
    Age Factors
    Amino Acid Transport System X-AG
    Animals
    Astrocytes
    Blotting, Western
    Clusterin
    *Complement Factor H
    Cytokines
    Disease Models, Animal
    Disease Susceptibility
    Fluorescent Antibody Technique
    Hippocampus
    Immunohistochemistry
    Inflammation
    Kainic Acid
    Male
    Microglia
    Neuroglia
    Random Allocation
    Rats
    Rats, Sprague-Dawley
    Seizures
    Severity of Illness Index
    Up-Regulation
    Neurology
    Pediatrics
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    Link to Full Text
    http://dx.doi.org/10.1111/j.1528-1167.2007.01135.x
    Abstract
    PURPOSE: Early-life seizures increase vulnerability to subsequent neurologic insult. We tested the hypothesis that early-life seizures increase susceptibility to later neurologic injury by causing chronic glial activation. To determine the mechanisms by which glial activation may modulate neurologic injury, we examined both acute changes in proinflammatory cytokines and long-term changes in astrocyte and microglial activation and astrocyte glutamate transporters in a "two-hit" model of kainic acid (KA)-induced seizures. METHODS: Postnatal day (P) 15 male rats were administered KA or phosphate buffered saline (PBS). On P45 animals either received a second treatment of KA or PBS. On P55, control (PBS-PBS), early-life seizure (KA-PBS), adult seizure (PBS-KA), and "two-hit" (KA-KA) groups were examined for astrocyte and microglial activation, alteration in glutamate transporters, and expression of the glial protein, clusterin. RESULTS: P15 seizures resulted in an acute increase in hippocampal levels of IL-1beta and S100B, followed by behavioral impairment and long-term increases in GFAP and S100B. Animals in the "two-hit" group showed greater microglial activation, neurologic injury, and susceptibility to seizures compared to the adult seizure group. Glutamate transporters increased following seizures but did not differ between these two groups. Treatment with Minozac, a small molecule inhibitor of proinflammatory cytokine upregulation, following early-life seizures prevented both the long-term increase in activated glia and the associated behavioral impairment. CONCLUSIONS: These data suggest that glial activation following early-life seizures results in increased susceptibility to seizures in adulthood, in part through priming microglia and enhanced microglial activation. Glial activation may be a novel therapeutic target in pediatric epilepsy.
    Source
    Epilepsia. 2007 Sep;48(9):1785-800. Epub 2007 May 23. Link to article on publisher's site
    DOI
    10.1111/j.1528-1167.2007.01135.x
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/43530
    PubMed ID
    17521344
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1111/j.1528-1167.2007.01135.x
    Scopus Count
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