Kainic acid-induced naip expression in the hippocampus is blocked in mice lacking TNF receptors

Charles Thompson, Devin Gary, Mark Mattson, Alex Mackenzie, George S. Robertson

Research output: Contribution to journalArticlepeer-review

Abstract

Mice that lack tumor necrosis factor-α (TNF) receptors are more susceptible than wild-type animals to brain injury produced by kainic acid or transient focal ischemia suggesting that the rapid production of TNF that occurs after these insults serves a neuroprotective role. The mechanisms by which TNF reduces neuronal loss after brain injury may involve the up-regulation of proteins that maintain calcium homeostasis or reduce free radical generation. We report here that systemic administration of kainic acid rapidly elevates expression of mRNA encoding neuronal apoptosis inhibitor protein (NAIP) in the hippocampus and that this increase does not occur in mice that lack TNF receptors. Given that NAIP overexpression can reduce neuronal injury by blocking apoptosis, our findings suggest that induction of the naip gene may contribute to the neuroprotective properties of TNF.

Original languageEnglish (US)
Pages (from-to)126-131
Number of pages6
JournalMolecular Brain Research
Volume123
Issue number1-2
DOIs
StatePublished - Apr 7 2004

Keywords

  • Apoptosis
  • Epilepsy
  • Hippocampus
  • Inflammation
  • Intracellular signaling pathways
  • Neuroprotection
  • Synaptic transmission and excitability

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience

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