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Inflammatory Response and Glia Activation in Developing Rat Hippocampus after Status Epilepticus
Author(s) -
Ravizza Teresa,
Rizzi Massimo,
Perego Carlo,
Richichi Cristina,
Velískǒvá Jana,
Moshé Solomon L.,
De Simoni M. Grazia,
Vezzani Annamaria
Publication year - 2005
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2005.01006.x
Subject(s) - status epilepticus , kainic acid , hippocampal formation , microglia , cytokine , hippocampus , western blot , immunocytochemistry , tumor necrosis factor alpha , epilepsy , neuroglia , biology , neuroscience , endocrinology , medicine , immunology , central nervous system , glutamate receptor , inflammation , receptor , biochemistry , gene
Summary: Purpose: We investigated the activation of microglia and astrocytes, induction of cytokines, and hippocampal neuronal damage, 4 and 24 h after kainic acid–induced status epilepticus (SE) in postnatal day (PN) 9, 15, and 21 rats. Methods: Limbic seizures were induced by systemic injection of kainic acid. Glia activation and neuronal cell loss were studied by using immunocytochemistry and Western blot. Cytokine expression was analyzed by reverse transcriptase–polymerase chain reaction (RT‐PCR) followed by Southern blot quantification. Results: After SE onset, hippocampal glia activation, cytokine expression, and neuronal damage are all age‐dependent phenomena. In the hippocampus, neuronal injury occurs only when cytokines are induced in glia, and cytokine synthesis precedes the appearance of degenerating neurons. Neuronal injury is more pronounced when interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) are produced in addition to IL‐1β. Conclusions: This study shows that cytokine induction in rat brain after sustained seizures is age dependent, and it is associated with the appearance of cell injury.