A sublethal dose of TNFα potentiates kainate-induced excitotoxicity in optic nerve oligodendrocytes

Brandon A. Miller, Fang Sun, Randolph N. Christensen, Adam R. Ferguson, Jacqueline C. Bresnahan*, Michael S. Beattie

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Glutamate receptor-induced cell death, known as excitotoxicity in both neurons and oligodendrocytes, has been implicated as a common pathway of cell death in numerous central nervous system (CNS) diseases and trauma. Research in both neuronal and oligodendrocyte excitotoxicity has examined glutamate's receptor-mediated effects on CNS cells, and explored strategies to protect cells exposed to the elevated glutamate levels that occur in CNS trauma and disease. Proinflammatory cytokines are also elevated in the injured CNS, and have also been implicated in CNS cell death. Recently, several laboratories have examined cytokines' effects on neuronal and glial excitotoxicity. Here, we review literature concerning the dynamic susceptibility of both neurons and oligodendrocytes to excitotoxicity, and present new data from our laboratory showing that the susceptibility of oligodendrocytes to excitotoxicity is acutely potentiated by the proinflammatory cytokine TNFα.

Original languageEnglish (US)
Pages (from-to)867-875
Number of pages9
JournalNeurochemical Research
Volume30
Issue number6-7
DOIs
StatePublished - Jun 2005
Externally publishedYes

Keywords

  • AMPA
  • Excitotoxicity
  • Glutamate
  • Oligodendrocyte
  • TNFα

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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