Inflammatory response and glia activation in developing rat hippocampus after status epilepticus

Teresa Ravizza, Massimo Rizzi, Carlo Perego, Cristina Richichi, Jana Velískǒvá, Solomon L. Moshé, M. Grazia De Simoni, Annamaria Vezzani

Research output: Contribution to journalArticle

131 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)113-117
Number of pages5
JournalEpilepsia
Volume46
Issue numberSUPPL. 5
DOIs
StatePublished - Jul 1 2005

Keywords

  • Brain development
  • Hippocamus
  • Interleukins
  • Neurodegeneration
  • Rat
  • Seizures

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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    Ravizza, T., Rizzi, M., Perego, C., Richichi, C., Velískǒvá, J., Moshé, S. L., De Simoni, M. G., & Vezzani, A. (2005). Inflammatory response and glia activation in developing rat hippocampus after status epilepticus. Epilepsia, 46(SUPPL. 5), 113-117. https://doi.org/10.1111/j.1528-1167.2005.01006.x